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PREFACE 


The  role  of  Endamoeba  buccalis  as  the  specific 
cause  of  pyorrhoea  alveolaris,  or  Riggs's  disease, 
has  very  recently  been  recognized.  It  happens,  as 
it  seldom  has  happened  before  in  the  history  of 
medicine,  that  whenever  the  specific  cause  of  the  dis- 
ease was  found,  a  specific,  eflficient  remedy  against 
the  parasite  was  already  known. 

This  infection  and  disease  is  so  wide-spread  that 
it  is  practically  universal,  and  is  the  cause  of  the 
loss  of  more  than  50  per  cent,  of  all  the  permanent 
teeth  that  are  lost  from  any  cause.  The  slow, 
incipient  nature  of  the  disease  results  in  its  pres- 
ence usually  not  being  suspected  until  consider- 
able irreparable  damage  has  been  done,  and  often 
not  until  many  teeth  are  practically  lost. 

The  most  successful  treatment  of  this  disease 
will  naturally  depend,  as  in  other  diseases,  largely 
upon  a  knowledge  of  the  specific  cause  of  the  disease, 
the  manner  in  which  this  agent  produces  the  dis- 
ease process,  and  finally  upon  a  knowledge  of  the 
manner  in  which  the  specific  treatment  acts  on  the 
causative  agent. 

13 


14  PREFACE 

The  object  of  this  book  is  to  present  the  sub- 
ject in  a  simple,  concise  way,  in  the  Hght  of  recent 
information.  Former  theories  and  ideas  as  to 
cause  and  treatment  are  left  out  altogether.  No 
attempt  is  made  to  include  a  review  of  the  liter- 
ature on  the  subject  except  in  so  far  as  it  may  seem 
essential  in  presenting  the  present  view. 

Though  diseases  involving  the  teeth  are  always 
of  special  interest  to  the  dentist,  pyorrhoea  alveo- 
laris,  with  its  long-drawn-out  suppurating  process 
in  the  mouth,  the  possible  effect  of  absorption  of 
infectious  and  toxic  substances,  and  the  harm 
that  may  come  from  being  unable  to  properly 
masticate  the  food,  is  of  special  interest  to  the 
physician  also.  The  book  is  intended  to  be  of 
practical  use  to  both  the  physician  and  the  dentist. 
It  is  also  believed  that  many  of  the  more  intelligent 
laymen  will  find  it  a  convenient  souice  of  informa- 
tion as  to  the  nature,  and  especially  the  preven- 
tion, of  this  disease,  from  which  all  sooner  or  later 
lose  their  teeth  if  they  live  long  enough. 

In  order  to  make  the  work  more  convenient 
when  required  for  quick  reference,  the  essential 
points  in  each  chapter  are  summarized  at  the 
end  of  the  chapter. 

The  Authors. 

New  Orleans,  La., 
May,  1915. 


CONTENTS 


CHAPTER  I 

Definition 17 

CHAPTER  n 

History 19 

CHAPTER  HI 

Etiology 26 

Summary 37 

CHAPTER  IV 

Morbid  Process 38 

Description  of  a  Tooth 39 

Endamebae  the  Specific  Cause 45 

Salivary  Calculus 69 

Serumal  Calculus Ji 

Change  of  Position  of  Teeth  from  Pyorrhea 71 

Loss  of  the  Alveolar  Process 73 

Summary j6 

CHAPTER  V 

Contagiousness 78 

Summary 81 

CHAPTER  VI 

Symptomatology 82 

Bleeding  from  Gums  the  Earliest  Symptom 83 

Soreness  of  Gums  and  Teeth  on  Pressure 84 

Bad  Taste  in  the  Mouth 85 

Foul  Breath 85 

Pyorrhea 86 

Sensitiveness  of  Neck  of  Tooth 87 

Retraction 87 

Looseness  of  the  Teeth 88 

Changes  in  Position  of  Teeth — Malocclusion ....  89 

Gum-boils 93 

Changes  in  the  Gums 93 

15 


i6  CONTENTS 


Absorption  of  Alveolar  Bone 96 

Summary 97 

CHAPTER  VII 

Diagnosis 99 

History - 99 

Microscopic  Examination loi 

Summary 118 

CHAPTER  VIII 

Treatment 120 

CHAPTER  IX 

Prophylaxis 144 

Summary 163 

Index 165 


ALVEOLODENTAL  PYORRHEA 


CHAPTER  I 
DEFINITION 

Many  terms  have  been  employed  to  designate 
the  disease  which  is  discussed  in  this  book.  Among 
them  are  pericementitis,  alveoHtis  dentahs,  alveo- 
lar periostitis,  Riggs's  disease,  Fouchard's  disease, 
and  pyorrhoea  alveolaris.  In  selecting  a  name  we 
have  taken  into  consideration  the  pathologic  proc- 
ess and  the  tissues  involved. 

The  term  pyorrhea  can  hardly  be  objected  to,  for 
there  is  pus  formation  and  flow  in  every  case  from 
the  very  incipiency  to  the  loss  of  the  last  tooth.  In 
the  smallest  lesions  the  amount  of  pus  produced 
may  be  so  small  as  to  require  microscopic  examina- 
tion to  demonstrate  it,  but  it  is  always  present. 
Later  the  quantity  becomes  much  greater,  coinci- 
dentally  with  the  increase  in  the  extent  of  the  lesion. 
The  term  pyorrhea,  however,  could  be  applied  to 
processes  in  which  there  is  pus  production  and  flow 
involving  other  structures  and  tissues  than  those  of 
the  mouth.  It  is  necessary,  therefore,  to  be  more 
specific  and  to  indicate  what  structures  are  in- 

2  17 


i8  ALVEOLODENTAL  PYORRHEA 

volved.  Pyorrhoea  alveolaris  is  perfectly  correct  in 
speaking  of  the  advanced  stage  of  the  disease,  but, 
as  will  be  seen  in  the  chapter  upon  Morbid  Process, 
the  pyorrhea  disease  exists  for  months  or  years 
before  it  involves  the  alveolar  bone.  During  this 
early  stage  the  peridental  soft  tissue  above  the 
level  of  the  alveolus  is  alone  involved.  The  term 
pyorrhcea  alveolaris  hardly  covers  this  early  stage 
of  the  disease.  At  the  time  when  the  cause  of  the 
disease  was  unknown  and  when  this  early  stage 
was  not  recognized  and  appreciated,  "pyorrhoea 
alveolaris"  met  the  requirements,  and  it  remains  a 
question  whether  usage  may  not  remove  any  ob- 
jection to  its  continued  use. 

The  word  alveolodental  means  pertaining  to  a 
tooth  or  teeth  and  to  a  socket  or  sockets.  Alveolo- 
dental pyorrhea  would  more  correctly  describe  the 
disease  under  consideration,  and  we  shall  employ 
it  in  this  book.  A  proper  definition  for  alveolo- 
dental pyorrhea  is,  "A  destructive  disease  of  the 
supporting  structures  of  the  teeth,"  and  we  may 
now  add,  "caused  by  Endamoeba  buccalis." 

Summary. — Alveolodental  pyorrhea :  A  destruc- 
tive disease  of  the  supporting  structures  of  the 
teeth,  the  specific  cause  of  which  is  Endamoeba 
buccalis. 


CHAPTER  II 
HISTORIC 

The  occurrence  of  minute,  unicellular,  ameboid 
organisms  has  been  a  matter  of  record  for  many 
years.  There  are  now  known  to  be  many  different 
classes  and  species.  Many  varieties  are  entirely 
free  living— feeding  on  smaller  animal  and  vege- 
table organisms  in  many  warm,  moist  places,  such 
as  in  ponds,  among  accumulations  of  decaying 
vegetation,  etc.  Other  varieties  live  and  repro- 
duce as  parasites  in,  or  upon,  the  higher  animals. 
Some  of  these  parasitic  amebae  are  most  probably 
only  harmless  commensals;  others,  by  their  con- 
stant occurrence  and  reactions  in  morbid  processes, 
are  now  thought  to  be  pathogenic,  either  directly 
or  indirectly.  At  present  we  are  chiefly  con- 
cerned with  the  species  known  and  described  as 
EndamxhcE  huccalis,  which  we  will  show  to  be 
constantly  present  in  the  lesions  of  alveolodental 
pyorrhea.  The  full  evidence  of  its  pathogenicity 
will  be  given  more  attention  in  the  succeeding 
chapters. 

As  far  back  as  1849,  when  this  form  of  life  first 
began    to    attract    attention,    Gros    described    an 

19 


20      .         ALVEOLODENTAL  PYORRHEA 

ameba  found  in  the  mouths  of  adults;  and  gave  it 
the  name  of  Amoeba  gingivalis. 

In  1862  Sternberg  gave  a  detailed  description 
of  an  ameba  found  mixed  with  the  deposits  of 
tartar  removed  from  the  teeth.  This  ameba 
differed  somewhat  from  the  ordinary  free-living 
ameba,  or  the  Amoeba  coli  found  in  other  parts  of 
the  alimentary  canal,  and  received  the  name  of 
Amoeba  buccalis. 

In  1879  Grassi  recorded  the  finding  of  an  ameba 
in  the  necrotic  material  from  carious  teeth,  to 
which  he  gave  the  name  of  Amoeba  dentalis. 

The  above  findings  were  restudied  by  Prowazek, 
when,  in  1904,  he  not  only  confirmed  the  described 
ameba  of  Sternberg,  but  redescribed  it  in  detail  in 
the  light  of  the  then  present  knowledge;  and  in 
one  of  the  first  attempts  at  the  classification  of  the 
various  forms  of  ameba  placed  it  in  the  class 
Entamoeba.  He  also  found  the  same  organisms 
present  in  scrapings  from  carious  teeth,  and  further 
concludes  that  all  amebae  that  had  been  described 
as  occurring  in  the  mouth,  except  Entamoeba  colij 
were  in  reality  the  same  species,  or  Entamoeba 
buccalis. 

Kartulis,  in  1900,  working  in  Egypt,  described 
an  ameba  found  in  suppurating  tumors  of  the 
jaw  which  he  thought  to  be  the  causative  agent. 
This  was  also  the  opinion  of  Doflein,  who  confirmed 


HISTORIC  21 

the  work  of  Kartulis,  and  named  the  organism 
Entamoeba  kartulisi.  Craig,  in  his  notable  work 
on  "The  Pathogenic  Amebae  of  Man,"  reviews  the 
descriptions  given  of  this  ameba,  and,  finding  that 
they  are  so  similar  to  the  "tetragena"  type  of 
E.  histolytica,  concludes  that  they  are  probably 
identical.  The  abscesses  referred  to  are  second- 
ary infections  from  a  preexisting  amebic  infection 
of  the  intestines.  Secondary  abscesses  as  a  sequel 
to  the  intestinal  infection  with  histolytica  often 
occur  in  the  liver,  brain,  bone,  etc. 

Recently,  in  July,  1914,  Smith  and  Barrett 
announced  at  a  meeting  of  the  Pennsylvania  State 
Dental  Society  the  finding  of  Endamceba*  huccalis 
in  nearly  all  cases  of  Riggs's  disease  (pyorrhoea 
alveolaris),  and  their  belief  that  the  organisms 
were  pathogenic  on  account  of  the  favorable  eff^ect 
on  the  lesions  of  the  disease  produced  by  the  local 
use  of  emetin  hydrochlorid,  a  well-known  amebicide. 

In  August  of  the  same  year  Dr.  Angelo  Chiavaro 
presented  a  paper  to  the  American  Dental  Society 
of  Europe  in  which  Endamoeba  buccalis  was  re- 
ported to  have  been  found  in  22  cases  of  pyorrhea, 

*  Throughout  the  remainder  of  this  book  the  term  endameba  is  used  in 
place  of  entameba,  proposed  by  Barbagallo  and  Casagrandi  in  1897,  because 
of  clear  historic  priority,  first  pointed  out  to  us  by  Allen  J.  Smith  (personal 
communication).  Endameba  was  proposed  for  a  parasitic  ameba  of  the 
cockroach  in  1897  by  Joseph  Leidy  (Proc.  Phila.  Acad.  Nat.  Sciences,  vol. 
xxxi,  p.  204),  eighteen  years  before  entameba  was  first  proposed  for  parasitic 
amebre  (Annali  d'Igiene  Sperimentele,  1897,  vol.  vii,  p.  103). 


22  ALVEOLODENTAL  PYORRHEA 

and  14  other  cases  not  affected,  out  of  a  total  of 
68  persons  examined.  This  author  concludes  that 
the  amebae  are  not  pathogenic,  but  were  in  reality 
an  adjuvant  to  the  auto-disinfection  of  the  mouth. 

Independently  of  the  work  of  these  last  two 
authors,  we  noted  the  occurrence  of  Endamceba 
buccalis  in  86  cases  of  unmistakable  alveolodental 
pyorrhea,  while  in  numerous  normal  controls  they 
could  not  be  found.  These  findings  were  reported 
to  the  Orleans  Parish  Medical  Society  in  Septem- 
ber, 1914,  at  which  time  we  expressed  the  opinion 
that  the  endamebae  were  pathogenic  for  many 
reasons,  chief  among  which  was  the  fact  that  they 
disappeared  and  the  lesion  promptly  began  to 
heal  upon  the  hypodermatic  administration  of 
emetin  hydrochlorid.  Again  in  February,  1915, 
in  the  Journal  of  the  American  Medical  Associa- 
tion, our  former  observations  were  confirmed  by 
further  observations  in  which  we  had  found 
endamebae  present  in  more  than  300  cases  of 
pyorrhea. 

Middleton  and  Barrett,  in  the  Journal  of  the 
American  Medical  Association  (vol.  Ixiii,  No.  20, 
p.  1746),  record  the  finding  of  Endamoehce  buccalis 
in  chronically  inflamed  tonsillar  tissue,  and  that 
the  condition  was  greatly  benefited  by  the  hypo- 
dermatic use  of  emetin. 

Up  to  the  present  time  there  is  no  conclusive 


HISTORIC  23 

evidence  that  any  pathogenic  ameba  has  been  cul- 
tivated artificially  either  in  pure  or  contaminated 
culture.  Thus  the  differentiation  of  the  various 
species  of  ameba  remains  a  comparative  study  of 
the  organism  along  structural  and  reproductive 
lines  in  general. 

In  the  large  series  of  cases  of  pyorrhea  that  we 
have  studied  all  the  organisms  appear  to  agree 
with  the  descriptions  given  for  Endamceba  huccalis 
except  that  occasionally  we  find  in  addition  an 
ameba  of  the  Endamceba  coli  type;  the  latter, 
particularly  in  preparations  from  the  surface  of 
the  lesion,  or  from  deposits  upon  the  buccal 
mucous  membrane. 

The  literature  bearing  upon  ameba  gives  bare 
mention  of  the  occurrence  of  this  very  common 
ameba,  probably  on  account  of  the  very  generally 
accepted  view  of  its  non-pathogenic  role.  In  his 
book,  ''The  Pathogenic  Amebae  of  Man,"  Craig 
gives  a  very  excellent  review  of  much  of  the 
important  literature  upon  this  organism.  It  is 
from  this  source  and  recent  observation  that  we 
have  compiled  the  following  brief  description  of 
Endamoebce  buccalis. 

Geographic  Distribution. — World-wide. 

Occurrence. — In  pyorrhea  lesions  around  the 
teeth   of   almost    all    human    adults    and    many 


24  ALVEOLODENTAL  PYORRHEA 

younger  people  and  also  in  the  follicles  of  diseased 
tonsils. 

Morphology. — Relatively  small.  Usually  from 
6  to  30  microns  in  diameter,  averaging  about  25 
microns.  The  ectoplasm  is  distinct  and  clear. 
The  endoplasm  is  granular  and  vacuolated,  having 
a  reticular  structure.  The  vacuoles  contain  vari- 
ous particles  of  phagocytized  material,  and  none 
of  them  are  contractile.  The  nucleus  is  well  de- 
fined, spherical  or  oval  in  shape,  and  has  a  thick 
nuclear  membrane  containing  refractile  material 
or  chromatin.  A  small  centriole  is  usually  situated 
near  the  center  of  the  nucleus. 

Motility. — ^This  is  somewhat  sluggish  in  character, 
and  is  produced  by  the  extrusion  of  ectoplasmic 
pseudopodia  into  which  the  endoplasm  is  drawn. 
The  motility  is  not  nearly  as  marked  as  E.  his- 
tolytica, but  more  so  than  E.  coli. 

Reproduction. — This  is  usually  accomplished  by 
simple  binary  fission — the  nucleus  dividing  by 
mitosis,  the  nuclear  spindle  often  being  observed. 
Schizogony  has  been  described. 

Cultivation. — There  are  no  records  of  successful 
cultivation.  A  personal  communication  from  A. 
J.  Smith  states  that  he  has  kept  the  organism  alive 
and  motile  for  twenty-four  hours  in  a  mixture  of 
equal  parts  of  egg-white  and  blood-serum. 

Pathogenicity. — Up  to  the  work  of  Smith  and 


HISTORIC  25 

Barrett,  and  later  our  own,  these  endamebae  have 
been  looked  upon  as  harmless  commensals.  The 
following  pages  will  deal  more  in  detail  with  this 
question. 

The  reader  is  referred  to  works  on  protozoology 
for  more  complete  and  scientific  description  of  this 
and  other  species  of  amebae  which  this  book  makes 
no  pretense  to  cover. 


CHAPTER  III 
ETIOLOGY 

Specific  Cause. — Endamebae,  of  the  species 
buccalisy  in  most  instances,  if  not  in  all,  are  present 
in  the  lesions  in  all  cases  of  alveolodental  pyorrhea. 
We  have  found  them  in  all  of  more  than  300  cases 
in  which  the  disease  had  developed  to  the  extent 
that  it  could  be  diagnosed.  In  two  cases  of  very 
early  disease,  in  both  of  which  the  diagnosis 
remains  in  doubt,  we  failed  to  find  endamebae. 
In  each  negative  case  only  one  examination  was 
made,  and  that  before  we  had  acquired  the  best 
technic. 

They  cannot  be  demonstrated  in  material  taken 
from  normal  gums.  They  are  often  found  in 
material  taken  from  gums  which  appear  on  casual 
observation  to  be  little  or  doubtfully  affected. 
Upon  more  careful  examination  with  proper 
instruments,  however,  pyorrhea  pockets  can  usu- 
ally be  demonstrated.  These  may  be  so  shallow 
as  to  be  doubtful,  but  more  often  they  are  much 
more  extensive  than  the  appearance  would  indicate. 
There  may  not  be  sufficient  pus  for  it  to  be  recog- 
nized by  the  unaided  eye,  but  in  every  instance 

26 


ETIOLOGY  27 

in  which  we  found  endamebae  many  pus-cells 
were  present  and  recognizable  with  the  aid  of  the 
microscope.  It  should.be  understood  that  a  con- 
siderable amount  of  pus  could  be  present  in  ma- 
terial, and  still  not  be  recognized  on  macroscopic 
examination. 

We  have  failed  to  find  endamebae  in  micro- 
scopic preparations  that  contained  no  pus,  and 
have  learned  to  discard  such  preparations  and  not 
to  waste  time  in  fruitless  search  for  endamebae  in 
them. 

Barrett  and  Smith  found  endamebae  in  all  of  46 
cases  of  pyorrhea,  and  did  not  find  them  in  7 
normal  mouths.  Chiavaro  found  them  in  all  of 
22  cases,  and  also  in  14  cases  not  diagnosed 
pyorrhoea  alveolaris.  This  is  to  be  explained  by 
the  reasonable  probability  that  he  did  not  consider 
the  diagnosis  indicated  until  the  disease  process 
had  reached  the  alveolar  level.  Strictly  speaking, 
pyorrhoea  alveolaris  must  involve  the  alveolar 
structure,  but,  as  is  shown  in  the  chapter  on 
Pathology,  the  early  stage  of  this  disease  is  pyor- 
rhoea dentalis,  which  later  extends  to  become 
pyorrhoea  alveolaris. 

The  constant  presence  of  endamebae  is  one 
argument  that  they  are  the  cause  of  the  disease, 
but  it  is  far  from  certain  proof  to  that  eff^ect. 
Another  important  bit  of  valuable  evidence  is  the 


28  ALVEOLODENTAL  PYORRHEA 

location  of  the  endamebae  in  the  lesions.  They 
are  much  more  numerous  in  the  depth  of  the 
lesion,  and  just  at  the  juncture  of  the  dead  and 
dying  tissue  with  the  living.  In  fact,  their  habitat 
(see  chapter  on  Pathology)  is  the  dying  tissue  in 
the  bottom  of  the  lesion,  where  bacteria  and  other 
agencies  are  few  or  entirely  absent.     This  fact  is 


-X— n 


Fig.  I. — Drawing  of  an  extracted  tooth  from  which  material  the  photo- 
micrographs, Figs.  2,  3,  4,  5,  and  6,  were  made.  A  part  of  the  peridental 
membrane  came  out  attached  to  the  roots,  and  is  indicated  by  the  large 
white  areas  with  ragged  edges. 

illustrated  by  the  pictures  on  pp.  28,  29,  30,  31. 
Other  evidence  that  the  endameba  is  the  specific 
cause  of  alveolodental  pyorrhea  is  the  very  certain 
and  rapid  results  that  follow  treatment  with  a  speci- 
fic amebicide.  It  might  be  argued  that  application 
or  injection  of  emetin  or  other  drugs  into  the  lesion 
might  benefit  by  some  local  healing  effect  or  by  kill- 
ing harmful  bacteria,  and  not  certainly  by  itsame- 


ETIOLOGY 


29 


H^n 

BL/i"^  - 

.rr-    ■'                 4 

^t, 

H^LJK  "jwv 

^ 

i  g;\          ^^L] 

"•■^^"v 

m 

#^ 

Mliii 

^^^mi^ 

«» ^  • 

Fig.  2. — Photomicrograph  of  representative  held  of  specimen  made  of 
material  removed  from  area  marked  I  in  Fig.  i.  Shows  pus  and  bacteria, 
but  no  endamebae. 


Fig.  3. — Photomicrograph  of  a  representative  field  of  specimen  made  of 
material  removed  from  area  marked  II,  Fig.  I.  Shows  pus,  bacteria,  and 
one  endameba. 


30 


ALVEOLODENTAL  PYORRHEA 


Fig.  4. — Photomicrograph  of  representative  field  of  specimen  made  from 
material  removed  from  area  marked  III,  Fig.  i.  Shows  pus,  bacteria,  and 
one  endameba. 


Fig.  5. — Photomicrograph  of  representative  field  of  specimen  made  of 
material  removed  from  area  marked  IV,  Fig.  I.  Shows  pus,  many  bacteria, 
and  three  endamebae. 


ETIOLOGY  31 

bicidal  action.  The  results  are  just  as  definite  and 
striking  if  the  drug  is  injected  hypodermatically 
into  some  part  of  the  body  remote  from  the  dis- 
ease. When  emetin  is  given  hypodermatically,  it 
is  diluted  so  much  by  the  blood  before  it  reaches 
the  seat  of  the  disease  until  it  has  certainly  lost 


Fig.  6. — Photomicrograph  of  representative  field  of  specimen  made  of 
material  removed  from  area  marked  V,  Fig.  i.  Shows  bacteria,  very  few 
pus-cells,  and  many  endamebae.  This  shows  how  much  more  numerous  the 
endamebae  are  in  the  very  bottom  of  the  lesion  at  the  edge  of  the  peridental 
membrane.     Could  there  be  greater  evidence  of  their  etiologic  r61e? 

all  its  possible  antibacterial  action,  though  not  its 
specific  amebicidal  power.  These  favorable  results 
are  coincident  with  the  disappearance  of  the  end-  \/ 
amebae.  The  bacteria  and  other  factors,  such,  for 
instance,  as  malapposition,  thought  by  some  to  be 
the  cause  of  the  disease,  are  not  affected. 
The  belief  that  endamebae  are  the  specific  cause 


32 


ALVEOLODENTAL  PYORRHEA 


of  the  disease  is  somewhat  strengthened  by  the 
similarity  of  the  lesion  and  the  relation  of  the 
parasites  to  it  as  compared  to  another  disease  of 
man,  amebic  dysentery,  caused  by  another  species 
of  endamebae.  The  parasites  are  most  numerous 
in  the  depth  of  the  undermined  ulcer  of  amebic 
dysentery  (see  Fig.  7),  just  as  they  are  most  num- 
erous in  the  very  depth  of  the  pyorrhea  lesion. 


Fig.  7. — Drawing  to  illustrate  amebic  ulcer  of  the  intestine.  Note  under- 
mined edges.  At  the  very  extremity  of  the  excavation  the  endamebae  are 
most  numerous.  Notesimilarity  of  the  lesion  to  that  of  alveolodental  pyor- 
rhea in  which  also  the  endamebae  are  most  numerous  and  active  in  the  very 
bottom  of  the  lesion. 


The  hemorrhagic  tendency  during  the  early  stage 
of  the  disease  is  also  like  amebic  dysentery. 

We  fully  appreciate  the  fact  that  Koch's  post- 
ulates have  not  been  satisfied  yet.  The  endamebae 
have  not  been  isolated  in  pure  culture,  injected 
into  another  individual,  thus  producing  the  disease, 
and  finally  reisolated  in  pure  culture.  We  would 
point  out  that  this  has  not  been  done  with  other 


ETIOLOGY  33 

diseases  due  to  protozoa.  In  fact,  it  was  impossible 
with  malaria  until  recently.  The  malarial  Plas- 
modium was  found  in  the  blood  of  all  cases  of 
malaria — it  was  not  present  in  the  blood  of  nor- 
mal individuals;  it  disappeared  coincidentally  with 
the  disease,  and  therefore  was  well  known  to  be 
the  specific  cause  of  malaria.  Endamebae  are 
present  in  all  lesions  of  all  cases  of  pyorrhea :  they 
are  not  present  in  normal  gums.  They  disappear 
when  the  lesions  get  well,  and  the  disease  gets 
well  when  the  endamebae  are  killed  by  a  specific 
amebicide.  We  have,  therefore,  fully  as  much 
evidence  of  specific  etiology  in  this  case  as  we  had 
in  malaria  ever  since  the  parasite  was  discovered, 
until  very  recently,  when  the  parasites  were  first 
cultivated  outside  of  the  body,  and  inoculation 
experiments  with  pure  culture  made  possible. 

Contributing  Factors. — ^Though  endamebae  are 
the  specific  cause  of  pyorrhea,  there  are  contri- 
buting factors,  one  or  more  of  which  are  thought 
to  be  almost  as  essential  as  the  endameba  itself. 
However,  these  would  be  quite  incapable  of  pro- 
ducing the  disease  in  the  absence  of  the  endamebae. 
Perhaps  the  most  important  of  these  is  trauma  or 
damage  to  the  gum  margin  involving  the  peri- 
dental membrane.  It  is  not  at  all  probable  that 
endamebae  would  produce  disease  or  could  affect 
the  normal  or  unbroken  tissue.     Damaged  tissue 

3 


34  ALVEOLODENTAL  PYORRHEA 

— favorable  soil — must  first  be  furnished  before 
the  infection  can  be  established.  Let  it  be  under- 
stood that  it  would  be  quite  possible  for  this 
favorable  soil  of  damaged  tissue  to  be  too  little 
for  its  existence  to  be  recognized  by  the  patient 
or  by  others.  It  might  be  microscopic  in  extent, 
and  still  be  amply  large  to  receive  many  endamebae. 
The  disease  affects  first  the  dental  periosteum  at 
the  attachment  of  the  gum  to  the  tooth.  It 
begins  in  the  tissue  between  the  teeth  most  fre- 
quently, and  therefore  those  things  most  likely 
to  damage  the  interdental  peridental  membrane 
would  be  the  greatest  source  of  harm.  No  doubt 
the  use  of  the  common  toothpick  is  a  very  common 
source  of  producing  the  traumatic  lesions  favor- 
able for  inoculation  of  endamebae.  We  are  not  at 
all  certain  but  that  the  use  of  dental  floss  for  the 
same  purpose  may  be  a  fruitful  source  of  harm  in 
this  same  way.  Unless  one  acquires  unusual 
skill,  it  very  often  damages  the  interdental  soft 
tissue,  and  bleeding  is  not  uncommon.  The 
bleeding  always  means  damaged  tissue.  The 
gum  attachment  may  also  be  damaged  while 
chewing  particles  of  food,  etc. 

Food-particles,  especially  hard  substances  forced 
between  the  teeth  and  resting,  making  pressure 
on  the  soft  edge  of  the  gum  if  allowed  to  remain  for 
sufficient  time,  cause  inflammation  and  ulceration 


ETIOLOGY  35 

of  the  tissue.  Such  diseased  tissue,  usually  in  the 
form  of  a  pocket,  would  furnish  ideal  soil  for  the 
inoculation  of  endamebae. 

We  are  inclined  to  think  that  tartar  allowed  to 
accumulate  on  the  teeth  by  insufficient  oral  hy- 
giene may  also  create  favorable  tissue  for  the 
establishment  of  endamebic  infection.  If  not 
removed,  it  continues  to  increase  until,  at  the 
gum  margin,  it  may  more  or  less  close  the  little 
groove  that  normally  exists  between  the  tooth 
and  the  very  edge  of  the  gum.  After  such  un- 
natural condition  is  established  small  particles  of 
food  that  may  get  into  this  more  or  less  closed 
groove,  by  their  pressure  and  decomposition, 
cause  inflammation  of  the  tissue.  Such  inflamed 
tissue  would  furnish  ideal  soil  for  endamebic  infec- 
tion. 

We  are  inclined  to  think  that  the  improper 
vigorous  brushing  with  a  stiffs  brush  may  also 
damage  the  gums  sufficiently  to  make  favorable 
damaged  tissue  for  infection  by  endamebae.  Brush- 
ing across  the  teeth  instead  of  from  gums  toward 
the  end  would  be  most  likely  to  do  harm. 

Crowns  forced  down  into  the  gum  are  a  source 
of  chronic  inflammation  and  finally  formation  of 
pockets  favorable  for  endamebic  infection.  Al- 
most all  the  crowns  we  have  examined  produce 
inflammation  of  the  gum,  usually  evidenced  by 


36  ALVEOLODENTAL  PYORRHEA 

redness,  and,  on  microscopic  examination,  pus 
formation.  We  do  not  know  whether  crowns 
could  successfully  be  used  without  their  being 
made  to  exert  pressure  on  the  gum.  We  think  that 
if  they  cannot,  the  advisability  of  their  use  is 
quite  doubtful. 

The  bacterial  flora,  including  spirochetae,  is 
also  very  probably  a  secondary  factor  in  bringing 
about  the  local  conditions  necessary  for  infection 
with  endamebae  and  also  in  the  progress  and  course 
of  the  disease.  There  is  a  great  variety  of  bac- 
teria in  the  mouth  of  most  individuals,  but  they 
vary  very  much  in  variety  and  numbers  with 
diff^erent  individuals,  being  influenced  largely  by 
the  care  taken  of  the  mouth  and  teeth.  Naturally, 
one  with  the  foulest  mouth  would  be  more  likely 
to  develop  a  favorable  pocket  for  endamebic  infec- 
tion following  trauma  to  the  gums,  than  one  who 
had  a  much  smaller  number  and  variety  of  bac- 
teria with  which  the  wound  would  promptly  be 
infected. 

Finally,  different  individuals  show  diff^erent  de- 
grees of  resistance  to  infections  of  various  sorts, 
and  there  is  no  reason  to  suppose  that  such  would 
not  be  the  case  also  in  this  infectious  disease. 


ETIOLOGY  37 

SUMMARY 

The  specific  cause  of  alveolodental  pyorrhea  is 
endamebae,  chiefly,  if  not  altogether,  of  the  species 
buccaHs.  They  are  present  in  all  lesions,  and  they 
are  not  present  in  the  absence  of  pyorrhea. 

Secondary  factors,  one  or  more  of  which  no 
doubt  are  essential,  are  trauma  or  wounding  of 
the  gums  at  the  point  of  attachment  to  the  teeth, 
lack  of  oral  hygiene,  and  possibly  individual 
resistance. 

Damage  to  the  gums  producing  favorable  soil 
for  infection  may  be  done  in  a  number  of  ways, 
among  which  are  picking  the  teeth,  cleaning  with 
hard  brushes,  floss,  rubbers,  and  the  effect  of  hard 
particles  of  food,  particles  of  food  betv\^een  the 
teeth  making  pressure  on  the  gums,  tartar  on  the 
teeth,  ill-fitting  crowns,  etc. 


CHAPTER  IV 

MORBID  PROCESS 

In  our  opinion,  it  is  of  vital  importance  for  all 
who  would  fully  understand  any  particular  phase 
of  this  disease — diagnosis,  prophylaxis,  or  treat- 
ment— first  to  familiarize  themselves  with  the 
morbid  process.  They  should  know  something 
of  the  structures  involved,  their  histology,  func- 
tions, etc.,  and  especially  how  such  tissues  break 
down  or  give  way  in  the  presence  of  the  disease, 
as  well  as  how  they  repair  whenever  the  cause  of 
the  disease  is  removed.  One  who  undertakes  to 
diagnose  the  presence,  or  especially  the  absence, 
of  the  disease  without  knowing  where  and  what  the 
disease  is,  is  likely  to  make  many  errors.  One 
who  looks  for  endamebae  without  knowing  some- 
thing of  the  kind  of  lesion  the  disease  produces 
and  where  the  endamebae  are  located  is  likely  to 
come  to  the  erroneous  conclusion  that  endamebae 
are  not  present  in  all  cases  of  pyorrhea,  as  we  say 
they  are.  One  who  undertakes  to  treat  the  disease 
without  having  some  idea  of  the  disease  process — 
how  it  is  produced  and  how  it  is  repaired,  as  well 
as  the  limits  of  nature's  ability  to  repair  the  tissues 

38 


MORBID  PROCESS  39 

involved — is  almost  certain  to  be  disappointed. 
It  will  be  necessary  for  us  to  present  a  brief  descrip- 
tion of  the  structures  involved,  but  only  in  so  far 
as  such  description  sheds  light  upon  the  disease 
itself.  It  should  be  understood  that  this  is  a 
disease  of  the  peridental  membrane,  but,  as  a 
result  of  damage  and  final  destruction  of  this 
tissue,  other  structures,  the  tooth  and  the  alveolar 
bone,  are  involved  also. 

DESCRIPTION  OF  A  TOOTH 

A  tooth  consists  chiefly  of  dentin,  a  very  hard 
substance.  The  crown  is  covered  with  a  harder 
substance,  the  enamel.  The  root  has  a  layer,  or 
several  layers,  of  cementum  covering  it.  The 
cementum  serves  to  attach  to  the  tooth  the  con- 
nective-tissue fibers  of  the  peridental  membrane 
which  hold  the  tooth  in  place.  Its  development 
depends  upon  certain  cells,  cementoblasts,  con- 
tained within  the  dental  portion  of  the  peridental 
membrane. 

The  Alveolar  Bone. — ^The  teeth  are  set  deeply 
in  sockets,  or  alveoli,  in  the  maxillae  and  mandible. 
The  outer  surface  of  the  alveolar  process  is  com- 
paratively smooth  and  covered  by  normal  peri- 
osteum. The  alveoli,  or  sockets,  into  which  the 
roots  of  the  teeth  fit,  are  bounded  by  a  thin,  definite 
bony  wall  which  is  pierced  by  a  great  many  open- 


40 


ALVEOLODENTAL  PYORRHEA 


ings.     The  surface  is  irregular.     These  cribriform 
plates  unite  the  cortical  plates  of  the  bone  at  the 


ii. a 


Fig.  8. — Drawing  to  illustrate  the  difFerent  structures  involved  in  alveolo- 
dental  pyorrhea:  A,  Gum  margin;  B,  alveolar  process;  C,  peridental  mem- 
brane; D,  cementum.  The  peridental  membrane  is  well  supplied  with 
blood-vessels,  and  the  alveolar  wall  is  very  irregular  in  outline. 


MORBID  PROCESS  41 

border  of  the  alveolar  process,  and  are  fused  with 
it  on  their  labial  and  lingual  sides.  They  are  really 
made  up  of  a  thin  layer  of  subperidental  bone, 
which  has  been  built  on  the  plates  of  cancellous 
bone  to  attach  the  fibers  of  the  peridental  mem- 
brane. 

Peridental  Membrane. — The    peridental    mem- 
brane is  the  soft  tissue  which  fills  the  space  between 


Fig.  9. —  Drawing  of  a  dissection  to  show  the  great  depth  to  which  the 
teeth  are  normally  set  in  the  bone.  It  necessarily  requires  a  long  time  for  a 
suppurating  process  to  remove  the  structures  shown  surrounding  the  teeth. 

the  surface  of  the  root  of  the  tooth  and  the  bony 
wall  of  its  alveolus,  surrounds  the  root  occlusally 
from  the  border  of  the  alveolus,  and  supports  the 
gum.  Its  chief  function  is  to  support  or  maintain 
the  tooth  in  proper  relation  to  adjacent  hard  and 
soft  tissues.  It  consists  largely  of  strong  con- 
nective-tissue fibers  running  in  various  directions 


42 


ALVEOLODENTAL  PYORRHEA 


and  at  various  angles  from  the  root  of  the  tooth 
to  the  wall  of  the  alveolus,  and  from  the  root  of 
the  tooth  into  the  gum.  By  fibers  running  from 
their  attachments  to  the  alveolar  wall  toward  the 
apex  of  the  tooth  the  tooth  is  suspended  or  swung 


__.t 


Fig.  lo. — Drawing  to  illustrate  the  peridental  membrane  and  its  continuity 
with  the  alveolar  periosteum. 

in  its  alveolus;  by  other  fibers  running  in  the 
opposite  direction  it  is  held  down  in  its  socket;  by 
still  others  it  is  held  from  turning  in  its  socket  in 
one  direction  or  another.  Later  we  shall  refer  to 
this  tough  connective-tissue  network  as  favorable 


MORBID  PROCESS  43 

tissue   for  long-continued   suppurating  processes, 


Fig.  II. — Drawing  suggesting  the  manner  in  which  the  tooth  is  suspended 
and  held  in  its  socket  by  connective-tissue  fibers  running  in  many  directions. 
A,  Alveolar  bone;  B,  cementum;  C,  fibers  of  peridental  membrane. 

and    especially  unfavorable   for  or  impossible  of 
regeneration. 


44 


ALVEOLODENTAL  PYORRHEA 


The  peridental  membrane  also  contains  blood- 
vessels, nerves,  and  certain  tissue-forming  cellsj 
osteoblasts  on  the  alveolar  side  and  cemento- 
blasts  on  the  side  next  to  the  root  of  the  tooth. 
These  are  capable,  under  favorable  conditions,  of 
forming  bone  or  cementum.     In  addition  to  these, 


Fig.  12. — Cross-section  of  a  young  tooth  showing  how  the  fibers  run  in 
different  directions,  preventing  the  tooth  from  turning  in  its  socket.  Con- 
traction of  these  fibers  pulls  the  tooth  to  one  side  or  twists  it  in  its  socket 
whenever  the  fibers  producing  the  opposite  action  have  been  destroyed  by 
the  pyorrhea  process. 

osteoclasts  are  also  present  and  capable,  under 
favorable  conditions,  of  removing  bone  or  cemen- 
tum. Under  the  age  of  maturity  there  are  also 
some  fibroblasts  present,  and  probably  capable, 
under  favorable  conditions,  of  making  new  con- 
nective-tissue fibers. 


MORBID  PROCESS  45 

ENDAMEBiE  THE  SPECIFIC  CAUSE 

As  is  discussed  more  fully  in  the  chapter  on 
Etiology,  endamebae  are  the  specific  cause  of 
alveolodental  pyorrhea.  The  disease  would  not 
occur  but  for  them.  On  the  other  hand,  we  do 
not  believe  it  possible  for  endamebae  to  attack 
successfully  the  normal  tissue  any  more  than 
tetanus  bacilli,  for  instance,  could  attack  the 
undamaged  tissue.  The  wide  distribution  of  these 
endamebae  (buccalis)  will  be  fully  discussed  in 
the  chapter  on  Prophylaxis.  Suffice  it  to  say 
here  that  the  infection  is  practically  universal. 
Practically  all  grown  people  have  them  in  pyor- 
rhea lesions  in  their  mouths,  and  many  younger 
people  have  them  also.  In  fact,  we  think  that 
almost  all  are  infected  before  they  are  twenty 
years  old.  Any  person  who  has  pyorrhea  is 
throwing  off  some  endamebae  in  the  saliva  all  the 
time.  All  our  associates,  including  the  immediate 
family,  are  a  source  of  infection,  as  well  as  many 
others  with  whom  we  do  not  come  in  so  direct 
association. 

These  endamebae  have  lived  for  countless  gener- 
ations in  pyorrhea  pockets  around  the  teeth  and 
some  other  locations.  Their  habitat  has  been, 
not  normal  tissue,  but  diseased  tissue.  Their 
food  and  other  requirements  have  been  supplied 


46  ALVEOLODENTAL  PYORRHEA 

in  this  particular  kind  of  diseased  tissue  for  count- 
less generations.  We  know  of  no  evidence  that 
these  parasites  live  in  nature  in  any  other  kind  of 
material.  Normal  tissue,  even  though  it  be  the 
mouth  and  gums,  would  be  very  far  from  being 
the  kind  of  material  this  parasite  is  accustomed 
to  live  in.  There  is  every  reason,  therefore,  to 
think  that  before  Endamoebae  buccalis  can  establish 
themselves  and  produce  their  disease,  the  proper 
peridental  tissue  must  be  damaged  so  as  to  produce 
favorable  soil  and  environment  for  them. 

Favorable  Soil. — Since  the  disease  is  practically 
one  of  peridental  membrane  only  we  may  ex- 
pect the  first  lesion  or  infection  in  any  given 
person  to  be  in  this  tissue.  There  are  many  ways 
in  which  damage  to  the  peridental  membrane  may 
be  produced.  It  is  to  be  understood  we  are  deal- 
ing with  a  very  small  microscopic  parasite,  no 
larger  than  many  of  the  tissue-cells  are.  There- 
fore it  is  not  necessary  that  the  lesion  produced 
should  be  large  enough  to  be  seen  with  the  unaided 
eye,  or  to  give  rise  to  pain  or  in  any  way  attract 
attention.  In  fact,  the  gum  and  peridental  mem- 
brane are  not  very  sensitive  to  pain.  Consider- 
able trauma  to  the  gum  may  be  produced  with- 
out much  pain  being  experienced. 

No  doubt  the  most  common  source  of  damage 
to  the  edge  of  the  peridental  membrane  is  hard 


MORBID  PROCESS  47 

particles  forced  against  it  and  efforts  to  remove 
particles  of  food  that  have  lodged. 

Normal  teeth  are  "self  cleaning,"  to  the  extent 
that  food  that  passes  between  them  gets  loose  as 
it  gets  nearer  to  the  gum.  Normally,  the  teeth 
come  closer  together  (in  fact,  touch)  near  the 
grinding  or  cutting  surface,  but  they  are  further 
apart  and  the  space  between  them  becomes  wider 
toward  the  attachment  of  the  gum  and  peri- 
dental membrane.  As  a  result  of  this,  food  forced 
between  them  in  biting  and  chewing  comes  out 
usually  without  any  effort  to  remove  it  being  nec- 
essary. In  spite  of  this  kind  provision  of  nature, 
hard  particles  of  food  may  occasionally  be  forced 
between  the  teeth  in  such  a  way  as  to  damage  the 
peridental  membrane  at  once  or  later,  as  a  result 
of  the  pressure  continually  made  against  the  soft 
tissue.  It  does  not  require  much  pressure  to  pro- 
duce inflammation  and  breaking  down  of  soft 
tissue  anywhere,  especially  if  aided  by  such  a 
bacterial  flora  as  is  always  to  be  found  in  the 
mouth. 

Efforts  to  remove  food  that  may  have  lodged 
between  the  teeth,  by  means  of  hard  instruments, 
such  as  toothpicks,  usually  damage  the  interdental 
soft  tissue.  How  often  does  one  pick  the  teeth 
without  breaking  the  continuity  of  tissue  at  some 
place  or  other  .^     Often  bleeding  is  produced  and 


48  ALVEOLODENTAL  PYORRHEA 

the  blood  is  seen  or  tasted.  Many  other  times  the 
damage  occurs,  but  is  not  sufficiently  great  to 
attract  attention  at  all.  In  fact,  even  whenever 
enough  trauma  is  produced  to  cause  noticeable 
quantities  of  blood  to  flow,  there  is  little  or  no 
pain  and  the  individual  does  not  realize  at  all  that 
any  harm  has  been  done. 

The  brunt  of  mastication  of  food  is  borne  by 
the  first  molar  and  the  teeth  just  in  front  and  just 
behind  it.  Damage  is  most  likely  to  occur  here, 
and  as  a  result  pyorrhea  generally  begins  around 
one  of  these  teeth.  These  teeth  are  also  generally 
lost  first.  The  examination  of  a  number  of  mouths 
will  bear  out  this  statement.  It  is  not  proposed 
for  a  single  moment  that  the  disease  may  not 
begin  around  any  other  tooth.  It  does  do  it  in 
many  instances. 

If  the  peridental  membrane  is  torn  loose  from 
the  tooth,  no  doubt  it  would  heal  back  in  a  very 
short  time  if  left  alone  and  given  an  opportunity. 
Healing,  however,  is  likely  to  be  interfered  with 
or  prevented  by  food  that  is  driven  into  the  space 
at  each  meal.  Small  particles  remain  and  act 
like  a  foreign  body,  not  only  irritating  and  pre- 
venting healing  directly,  but  they  favor  the  growth 
and  harmful  action  of  bacteria  which  are  always 
present  in  the  mouth.  Such  a  lesion  containing 
food-particles  and  bacteria  will  have  some  pus- 


MORBID  PROCESS  49 

cells  in  it  within  twenty-four  hours,  and  if  healing 
is  prevented  by  repeatedly  forcing  food  into  it,  it 
soon  becomes  ideal  soil  for  an  Endamceba  buccalis, 
if  one  should  chance  to  be  planted  there.  Of 
course,  as  long  as  an  individual  has  no  focus  of 
infection  in  his  own  mouth  as  a  source  of  endamebae 
and  must  depend,  therefore,  upon  outside  sources, 
the  chances  of  a  particular  traumatic  lesion  getting 
infected  are  not  great.  If  such  a  wound  does 
not  get  infected  with  endamebae,  it  heals  in  a  few 
days,  as  soon  as  nature's  reacting  and  healing 
powers  have  time  to  accomplish  this  result.  The 
bacteria  and  irritation  by  food  are  not  sufficient 
to  prevent  healing  in  a  few  days,  any  more  than 
they  would  prevent  healing  of  other  lesions  involv- 
ing other  tissues  in  the  mouth. 

The  First  Lesion  a  Source  of  Infection  to  Others. 
— Let  us  suppose  that,  on  account  of  the  character, 
size,  or  location  of  the  lesion  or  some  other  influence 
a  lesion  or  little  pocket  by  the  side  of  a  tooth  did 
not  heal  promptly,  and  did  get  infected  with 
endamebae.  These  endamebae  multiply  rapidly 
and  crawl  about  from  place  to  place,  by  their 
ameboid  movement  burrowing  about  among  the 
granulations  and  inflamed  tissue  of  the  lesion,  and 
actually  penetrate  the  diseased  tissue.  It  is  quite 
probable  that  they  are  in  search  of  some  particular 
4 


^ 


50  ALVEOLODENTAL  PYORRHEA 

kind  of  cell  or  product  of  the  inflammatory  process 
for  their  food. 

Pus  from  various  sources,  including  that  from 
pyorrhea  lesions,  contains  certain  cells  or  portions 
of  cells  which  usually  contain  a  very  dark-staining 
nucleus.  In  fact,  such  bodies  may  be  found  in 
most  any  pus  from  chronic  inflammatory  lesions. 
These  same  bodies  are  found  quite  regularly  in 
Endamoeba  buccalis.  Frequently  one  endameba 
may  contain  as  many  as  eight  or  ten  of  them. 
They  appear  to  be  the  food  of  the  endamebae. 
These  bodies  are  comparatively  few  in  number, 
and  are  mixed  or  distributed  among  the  pus-cells. 
In  order  for  an  endameba  to  secure  them  it  would 
be  necessary  for  the  parasite  to  move  about  in  the 
material  containing  them — to  forage,  as  it  were, 
for  them.  Endamebae  thus  move  about  back  and 
forth  over  the  ulcerated  surface  and  among  the 
granulations  of  the  lesion.  It  is  not  known 
whether  they  damage  directly  or  attack  the  living 
tissue,  but  it  is  not  at  all  necessary  for  them  to  do 
so  for  them  to  be  pathogenic.  They  may  produce 
great  harm  and  actually  be  the  essential  cause  of 
the  pyorrhea  by  continually  carrying  and  plant- 
ing and  replanting  harmful  bacteria  in  the  tissue. 

Though  endamebae  are  small,  microscopic  ob- 
jects, the  largest  of  them  are  many  hundred  times 
larger  than  the  small  bacteria  of  different  kinds 


MORBID  PROCESS  51 

present  also  in  the  lesion.  These  bacteria  are  not 
capable  of  preventing  healing  themselves,  because 
the  resisting  powers  of  the  tissues  and  body  fluids 
keep  them  walled  off  or  pushed  back  out  of  the 
living  tissue.  The  endamebae,  however,  carry 
them  in  and  out  of  the  granulation  tissue  as  they 
move  about  in  it.     Bacteria  can  be  seen  on  and 


Fig.  13. — Drawing  of  actual  observation  of  Endamoebae  buccalis  passing 
through  a  narrow  place  between  cells.  Note  mass  of  bacteria  being  drawn 
with  it.  In  this  manner  they  carry  and  plant  bacteria  in  the  granulation 
tissue  of  the  lesion. 


in  moving  endamebae  by  watching  them  under 
the  microscope.  One  can  see  endamebae  transport 
bacteria  from  one  place  to  another  in  the  prepara- 
tion, and  it  would  seem  reasonable  to  suppose  that 
they  do  the  same  thing  in  the  diseased  tissue. 

Bacteria  that  are  being  continually  carried  and 
planted   into   the   diseased   tissue   could   thus   do 


52  ALVEOLODENTAL  PYORRHEA 

much  more  damage  than  if  they  were  not  aided. 
One  effect  they  surely  have  is  to  cause  the  produc- 
tion of  pus  if  they  are  pyogenic  bacteria.  It  would 
seldom  occur  that  such  a  lesion  would  not  have 
some  pyogenic  species.  No  doubt  the  kind  of 
secondary  bacteria  present  influences  the  amount 
of  pus  produced  in  a  given  case,  and  to  a  great 
extent  the  course  of  the  disease. 

In  addition  to  bacteria,  there  are  also  different 
species  of  spirochetes  present  in  the  mouth,  and 
these  are  often  very  numerous  in  pyorrhea  lesions. 
There  is  good  reason  to  believe  that  they  may  also 
be  important  secondary  factors  in  most  cases. 

We  do  not  know  of  any  conclusive  evidence  that 
the  endamebae  do  or  do  not  directly  damage  or 
break  down  tissue.  It  is  quite  possible  that  they 
could  not  produce  pyorrhea  unaided  by  their 
symbiotic  bacteria  and  spirochetes,  any  more 
than  the  bacteria  and  spirochetes  can  produce  the 
disease  unaided  by  the  endamebae.  There  are 
many  instances  of  such  obligatory  symbiosis  in 
nature.     This  is  a  subject  for  future  investigation. 

After  one  such  focus  of  infection  is  established, 
from  which  endamebae  are  being  thrown  off  into 
the  mouth  all  the  time,  a  favorable  lesion  produced 
by  subsequent  damage  to  the  peridental  membrane 
around  other  teeth  is  much  more  likely  to  become 
infected.     The    larger    the    number    of    infected 


MORBID  PROCESS  53 

lesions,  the  more  probable  it  becomes  that  when- 
ever other  lesions  are  produced  they  will  get 
infected.  It  is  here  seen  how  important  it  is  to 
prevent  the  first  infection,  which  is  almost  certain 
to  occur  during  childhood.  Unfortunately,  our 
former  knowledge  of  the  disease  only  led  to  inter- 
est and  concern  in  the  disease  in  older  people  after 
they  began  to  lose  their  teeth  or  were  about  to  do 
so.  Now  that  we  know  the  specific  cause  of  the 
disease,  that  it  is  contagious,  and,  fortunately,  how 
to  prevent  the  establishment  of  the  infection, 
there  is  no  doubt  that  dissemination  of  this  knowl- 
edge will  lead  to  the  prevention  of  this  unneces- 
sary veritable  scourge  of  man,  to  a  great  extent. 
The  importance  of  preventing  the  primary  in- 
fection cannot  be  emphasized  too  forcibly.  One 
who  has  no  endamebae  in  his  mouth  would  not 
be  in  much  danger  of  getting  wounds,  that  chance 
to  be  produced,  infected  with  endamebae.  It  must 
be  quite  an  accident  for  the  first  endameba  to 
get  planted  or  lodged  in  a  wound  in  the  edge  of 
the  peridental  membrane.  The  number  intro- 
duced into  the  mouth  from  without  must  be  com- 
paratively small.  Sooner  or  later,  however,  the 
accident  happens.  After  the  endamebae  are 
established  in  one  pyorrhea  lesion  there  is  a  con- 
stant overflow  of  them  into  the  mouth.  They  can 
be  identified  in  the  saliva  of  advanced  cases  with 


54  ALVEOLODENTAL  PYORRHEA 

ease.  By  first  diluting  the  material  and  then 
centrifuging,  we  recovered  ii  endamebae  from  a 
single  mouthful  of  "spit"  in  one  instance.  Not 
only  is  such  a  person  likely  to  be  a  source  of  infec- 
tion to  others,  but  he  is  a  fruitful  source  of  infec- 
tion to  himself,  or'  rather  of  spreading  infection 
in  his  own  mouth. 

The  Course  of  the  Disease  in  a  Given  Lesion. — 
Whenever  the  disease  is  established,  its  course 
and  progress  vary  considerably,  dependent  upon 
many  variable  factors.  The  lesion  at  first  con- 
sists of  a  small  pocket  by  the  side  of  the  tooth. 
The  tooth  from  which  the  peridental  membrane 
was  torn  makes  one  side  of  the  pocket,  while  the 
rest  of  its  wall  consists  of  inflamed  granulation  or 
ulcerated  tissue — an  ulcer  held  against  the  tooth. 
One  side,  however,  is  open  and  permits  the  out- 
flow of  pus.  Depending  upon  the  location  of  the 
lesion,  it  will  be  more  or  less  subject  to  food  being 
forced  into  it.  Food-particles  are  a  source  of 
increased  inflammation  and  bacterial  growth,  and 
no  doubt  they  contribute  to  the  progress  of  the 
disease  in  many  instances.  Usually,  however, 
many  months  or  even  years  pass  before  the  disease 
has  destroyed  the  peridental  membrane  as  far  as 
the  edge  of  the  alveolar  bone.  The  pocket  gets 
deeper  and  wider,  and  more  and  more  pus  is  pro- 
duced because  of  the  increased  ulcerated  surface. 


MORBID  PROCESS 


55 


The  gum  is  red  and  inflamed  whenever  the  lesion 
is  on  the  labial  or  lingual  side  of  the  tooth  in  most 


Fig.  14. — Drawing  to  illustrate  an  early  pyorrhea  lesion  by  the  side  of  a 
tooth.  The  disease  has  just  reached  the  level  of  the  alveolar  process,  which 
is  almost  exposed. 

instances,  but  in  others  casual  observation  hardly 
detects  that  it  is  abnormal.  The  disease  begins 
much  more  frequently  between  the  teeth,  but  the 


S6 


ALVEOLODENTAL  PYORRHEA 


interdental  soft  tissue  is  not  so  likely  to  appear  red 
and  inflamed.     In  fact,  it  is  only  by  careful  exam- 


Fig.  15 — Drawing  to  illustrate  a  more  advanced  stage  of  pyorrhea  by  the 
side  of  a  tooth.  The  peridental  membrane  has  been  destroyed  for  a  consider- 
able distance  down  the  alveolus.  The  bone  has  begun  to  be  removed,  and 
the  gum  to  retract  as  the  bone  gives  way.  Whenever  the  progress  of  the 
disease  is  rapid,  the  alveolar  bone  is  laid  bare. 

ination  with  a  suitable  instrument  that  some  of 
the  small   lesions   between   the   teeth   are  found. 


MORBID  PROCESS  57 

One  is  in  doubt  often  until  he  examines  the  material 
removed  from  a  suspected  lesion  microscopically 
and  finds  pus-cells  and  endamebae. 

During  this  early  stage  the  gum  bleeds  easily 
from  slight  trauma,  such  as  picking  the  teeth, 
brushing  them,  sucking  air  between  them,  etc. 
The  cause  of  this  tendency  to  bleed  readily  is 
the  granulation  surface  or  ulcer.  Granulations  in 
other  tissues  of  the  body  bleed  from  slight  trauma 
in  the  same  way.  The  lesion  probably  seldom 
ever  entirely  encircles  the  tooth-root  at  this  stage, 
though  this  sooner  or  later  occurs  in  most  instances. 
We  have  seen  instances,  however,  where  the 
disease  extended  to  the  very  end  of  the  root  on  the 
side  next  to  another  diseased  tooth,  while  the 
opposite  was  well  and  the  interdental  soft  tissue 
intact  and  normal. 

Up  to  this  time  there  is  little  or  no  pain  pro- 
duced. The  tissue  involved  is  not  very  sensitive 
to  pain.  There  may  be  considerable  discomfort 
and  uneasy  feeling,  especially  following  a  meal, 
produced  by  particles  of  food  forced  into  the 
pocket  (or,  as  is  usually  the  case,  pockets)  or  held 
against  the  diseased  tissue  between  the  teeth. 
This  leads  to  picking  the  teeth  or  effort  to  remove 
food  in  other  ways.  Many  have  been  educated 
up  to  passing  a  cord  or  dental  floss  between  the 
teeth  for  this  purpose.     This  is  probably  fully  as 


58  ALVEOLODENTAL  PYORRHEA 

harmful  as  picking  the  teeth,  because  it  is  seldom 
done  without  traumatizing  the  interdental  soft 
tissue. 

After  the  disease  has  existed  long  enough,  there 
begins  to  be*  more  or  less  retraction  of  the  gum, 
leaving  exposed  dentin  which  is  often  sensitive  to 
changes  of  temperature  and  physical  force.  Hold- 
ing hot  or  cold  water  about  the  teeth  or  forcing 
it  between  them  gives  rise  to  pain.  This  may  be 
noticed  for  months  or  years  before  the  patient 
realizes  that  pyorrhea  exists. 

Though  the  disease  begins  around  a  single  tooth, 
it  is  unusual  to  find  people  over  twenty  years  old 
who  haven*t  more  than  one  tooth  involved.  We 
have  seen  patients  in  whom  we  could  demonstrate 
lesions,  pus,  and  endamebae  around  every  tooth 
in  their  mouth.  It  is  common  to  find  the  disease 
around  at  least  four,  six,  eight,  or  ten  teeth  in  the 
same  individual.  Of  course,  the  lesions  are  of 
diff^erent  shape  and  extent  around  different  teeth. 

Peridental  membrane,  being  composed  chiefly 
of  tough  fibers,  is  destroyed  slowly  by  suppu- 
rative processes.  Finally,  however,  the  pocket 
reaches  the  level  of  the  alveolar  bone.  The 
destructive  process  continues  in  the  peridental 
membrane  now  between  the  tooth  and  the  wall 
of  the  alveolus.  As  it  progresses  the  peridental 
membrane  is  gradually  sloughed  or  eaten  away. 


MORBID  PROCESS  59 

In  case  of  a  rapidly  progressing  disease  the  pocket 


Fig.  16. — Drawing  to  illustrate  the  last  stage  of  a  pyorrhea  lesion  by  the 
side  of  a  tooth.  The  peridental  membrane  has  been  entirely  destroyed, 
except  a  small  portion  in  the  very  bottom  of  the  socket  (not  shown  here) 
which  is  still  holding  the  tooth  in  place.  There  has  been  great  destruction  of 
alveolar  bone  and  consequent  retraction  of  the  gum.  The  rapid  destruction 
results  in  considerable  exposure  of  the  bone. 

now  has  bare  tooth-root  on  one  side  and  bare 
alveolar  bone  on  the  other,  with  ulcerated  gum 


6o 


ALVEOLODENTAL  PYORRHEA 


at  its  edge  and  the  granulating,  ulcerated  edge 
of  peridental  membrane  in  the  bottom.     Figs.  14, 


■'J 

Fig.  17. — Early  stage  of  slowly 
progressive  disease.  The  bone  is 
not  laid  bare  at  any  time. 


<V'^f3  o. 


Fig.  18. — Drawing  to  illustrate 
more  advanced  stage  of  slowly  pro- 
gressing disease.  The  bone  has  been 
absorbed  as  the  disease  progressed. 


15,  and  16  illustrate  such  lesions.     In  the  usual 
slowly  progressing  lesion,   however,   the   bone   is 


MORBID  PROCESS  6i 

absorbed  as  the  lesion  extends  and  is  not  exposed 
or  denuded  of  all  soft  tissue.  Figs.  17,  18,  and  19 
represent  such  lesions.  Large  numbers  of  end- 
amebae  are  demonstrable  on  and  in  this  latter 
granulating  tissue.  The  pocket  contains  food 
particles  that  have  been  forced  into  it,  myriads 
of  bacteria  and  spirochetes,  much  pus,  and  many 
endamebae.  The  latter,  however,  are  much  more 
numerous  in  the  very  bottom  of  the  lesion,  and 
this  point  should  be  kept  in  mind  when  examining 
for  them. 

The  decomposing  contents  of  the  pocket  neces- 
sarily have  a  bad  odor.  This  varies  with  the  bac- 
terial flora  present,  some  giving  rise  to  different 
and  stronger  odors  than  others.  Certain  spiro- 
chetes contribute  largely  to  the  odor  of  the  con- 
tents of  pyorrhea  pockets.  During  the  hours 
when  one  is  awake  and  the  mouth  is  being  worked, 
the  material  does  not  accumulate  so  much,  and 
therefore  the  decomposition  is  not  so  great.  Dur- 
ing sleep  and  quiet  pus  accumulates,  and  the 
decomposition  with  resultant  odor  is  greater.  It 
is  sufficient  to  give  rise  to  a  foul  breath  and  often 
a  bad  taste  in  the  mouth.  The  bad  taste  in  the 
morning  is  largely  due  to  this  material.  The 
thought  would  distress  many  people  if  they  knew 
how  much  pus,  and  what,  they  were  swallowing 
each  day — and  up  to  now  there  has  been  no  escape 


n 


62  ALVEOLODENTAL  PYORRHEA 

from  it.  Some  people  lose  their  teeth  earlier  than 
others,  but  all  lose  them  from  this  suppurating 
process  sooner  or  later.     Some  happen  to  have 


Fig.  19. — Drawing  to  illustrate  still  more  advanced  or  final  stage  of 
slowly  progressing  disease.  Peridental  membrane  destroyed  to  the  very 
apex  of  the  root  and  alveolar  bone  entirely  gone  on  one  side.  Such  a  tooth 
is  loose  and  usually  falls  out  of  normal  position. 

different  bacterial  flora  in  their  mouths  or  they 
have  different  spirochetes,  and  therefore  their 
breath  is  worse  than  that  of  others,  or  they  have 


MORBID  PROCESS  63 

more  pus  than  others,  but  it  is  a  question  of  degree 
only.  It  cannot  be  said  that  foul  breath  is  due 
to  pyorrhea  altogether,  but  it  is  practically  so.  If 
everybody's  breath  smelled  to  himself  like  it  does 
to  the  other  fellow,  and  if  it  was  known  by  all  that 
the  odor  results  chiefly  from  pyorrhea,  it  is  doubt- 
ful whether  there  would  be  enough  ipecac  pro- 
duced in  South  America  and  India  combined  to 
supply  the  demand! 

The  destructive  process  continues,  and  finally 
the  peridental  membrane  that  remains  is  insuffi- 
cient to  hold  the  tooth  rigid  in  the  socket.  It  gets 
loose  and  can  be  moved  from  side  to  side  with 
little  force.  It  continues  to  get  looser  and  looser 
during  several  months  or  years  until  it  finally 
falls  out,  or,  as  is  usually  the  case,  it  is  removed 
artificially  on  account  of  pain  or  worry  that  it  may 
cause.  Sometimes  a  tooth  will  hang  on  for  several 
years  after  it  has  gotten  loose. 

The  socket  enlarges  as  a  result  of  slow  absorp- 
tion of  the  alveolar  bone,  which  is  denuded  of  peri- 
dental membrane.  It  is  constantly  bathed  in  pus, 
but  it  is  doubtful  whether  it  is  removed  as  rapidly 
as  by  nature  when  a  tooth  that  has  not  been  pre- 
viously diseased  with  pyorrhea  is  extracted.  In 
the  former  instance  it  usually  requires  many 
months  for  complete  absorption  of  the  alveolar 
process.     In  pyorrhea  the  removal  of  the  alveolar 


64  ALVEOLODENTAL  PYORRHEA 

process  goes  on  during  the  time  the  tooth  remains 
after  the  bone  begins  to  be  stripped  of  its  peri- 
dental membrane.  Frequently  the  removal  of 
bone  has  been  very  great  before  the  tooth  is  finally 
lost  (Fig.  19).  As  the  bone  is  removed  the  gum 
retracts,  and  frequently  half  the  length  of  the  root. 


Fig.  20. — Photograph  of  postmortem  specimen  showing  great  retraction 
of  gum,  with  consequent  exposure  of  roots  of  teeth,  in  a  case  of  pyorrhea  of 
long  duration.  Some  people's  teeth  hold  fast  much  longer  than  others  do  in 
the  presence  of  the  disease. 

or  even  more,  stands  above  the  level  of  the  gum 
before  the  tooth  finally  comes  out  (Figs.  20  and  21). 
Sometimes  the  disease  results  in  more  or  less 
destruction  of  the  periosteum  covering  the  edge 
of  the  alveolar  bone,  in  which  instance  there  may 
be  considerable  caries.     This  leads  to  thickening  of 


MORBID  PROCESS 


65 


the  gum  over  the  edge  of  the  bone.     Where  there 
is  much  carious  bone,  the  heahng  process  follow- 


Fig.  21. — The  lingual  side  of  the  same  specimen  shown  in  Fig.  20. 


Fig.  22. — Skiagraph  of  normal  teeth  showing  the  interdental  alveolar  bone 
(Courtesy  of  Dr.  C.  Edmond  Kells). 

ing  the  falUng  of  a  tooth  is  very  slow.     The  gum 
over  it  remains  thick  for  many  months.     Where 


66  ALVEOLODENTAL  PYORRHEA 

there  is  little  caries,  the  disease  stops  and  the 
socket  soon  heals  up.  We  do  not  know  what 
becomes  of  the  endamebae,  but  it  is  probable  they 


Fig.  23. — Skiagraph  showing  disappearance  of  alveolar  process.  Note 
how  little  support  the  teeth  have.  This  lost  bone  cannot  be  regrown.  The 
teeth  now  lean  to  one  side  for  lack  of  support. 


Fig.  24. — Skiagraph  showing  loss  of  alveolar  bone  from  pyorrhea. 

disappear  from  the  particular  socket  because  there 
is  no  peridental  membrane  left  for  them  to  live 
in.     This  is  their  natural  habitat. 


MORBID  PROCESS  67 

Amount  of  Blood  and  Pus  Lost  During  the 
Course  of  the  Disease. — It  is  interesting  to  specu- 
late on  the  amount  of  blood  and  pus  lost  during 
the  course  of  the  disease.  If  one  sucks  or  picks 
or  brushes  the  tooth  during  the  early  stage  of  the 
disease,  a  drop  or  two  of  blood  oozes  out  in  many 
instances.  This  is  noticed  by  the  patient,  but 
perhaps  it  is  done  only  once  or  twice  a  day.  Some 
people  get  much  larger  quantities  from  their  teeth. 
In  fact,  some  bleed  without  any  trauma  at  all. 
True,  others  have  little  bleeding.  There  is  a 
very  much  larger  amount  of  blood  caused  to  flow 
by  chewing  food.  It  is  mixed  with  the  food  and 
not  noticed.  One  who  has  bleeding  gums  makes 
them  bleed  whenever  he  masticates  food  until 
they  "bleed  out."  This  is  repeated  at  every 
meal.  Many  people  waste  one  to  several  drams 
of  blood  in  this  way  every  day  for  weeks,  months, 
and  years.  Though  the  loss  of  such  a  small 
quantity  of  blood  for  a  short  time  only  could 
hardly  be  considered  likely  to  be  very  harmful,  it 
is  quite  probable  that,  kept  up  for  a  sufficient 
length  of  time,  it  may  be  a  source  of  much  harm. 
Only  three  drams  a  day  for  a  year  would  be 
about  a  gallon,  and  it  is  not  at  all  improbable 
that  the  loss  of  a  gallon  of  blood  each  year  would 
be  harmful. 

As  for  the  pus,  one  can  obtain  one  or  two  drops 


68  ALVEOLODENTAL  PYORRHEA 

from  a  pyorrhea  pocket  by  massaging  it,  and  after 
five  or  six  hours  a  similar  amount  can  be  obtained. 
It  is  not  a  high  estimate  to  say  that  at  least  four 
drops  of  pus  can  be  secured  from  the  average  pyor- 
rhea pocket  during  twenty-four  hours.  When 
mixed  with  the  saliva  in  driblets  and  swallowed,  it 
is  not  noticed,  however.  This  would  be  an  ounce 
in  one  hundred  and  twenty  days,  or  three  ounces  in 
a  year.  We  believe  it  would  be  a  very  conservative 
estimate  to  say  that  the  average  tooth  suppurates 
more  than  ten  years  before  it  is  finally  removed 
by  pyorrhea.  Thus  about  one  quart  of  pus  would 
be  produced  for  each  tooth,  and  for  all  32  teeth, 
about  eight  gallons.  The  disgusting  thought  about 
it  is  that  all  this  eight  gallons  of  pus  is  produced 
in  the  mouth  and  that  most  of  it  is  swallowed.  It 
would  be  no  great  surprise  if  the  production  and 
loss  of  this  large  amount  of  pus  should  have 
marked  harmful  influence  on  the  health  and  per- 
haps the  longevity  of  the  individual. 

That  this  disease  may  influence  the  longevity  of 
individuals  by  the  loss  of  their  teeth  and  the 
resulting  failure  to  masticate  and  digest  their  food 
well  can  hardly  be  doubted.  In  fact,  it  will  be 
conceded.  This,  coupled  with  the  probable  harm- 
ful influence  of  the  loss  of  blood  and  pus,  serves  to 
indicate  that  the  disease  now  under  discussion  is 
of  vast  importance  to  all  humanity.     Think  what 


MORBID  PROCESS  69 

it  would  mean  in  comfort,  health,  pleasure,  and 
longevity  to  man  if  this  veritable  scourge  could 
be  blotted  out!  What  a  different  people  we  would 
have  if  all  retained  and  enjoyed  their  teeth  as  long 
as  they  lived!  At  present  the  average  person 
begins  to  get  along  without  a  part  of  his  teeth  or 
substitutes  artificial  ones  by  the  time  half  of  his 
life  is  spent.  During  the  remaining  half  of  life 
this  disease,  consisting  of  a  filthy,  sloughing  proc- 
ess in  the  mouth,  slowly  but  surely  removes  the 
remaining  teeth,  which  the  better-to-do  may  sub- 
stitute with  artificial  teeth, — a  poor  makeshift, — 
but  the  majority  have  to  "gum  it"  as  long  as  they 
live.  Think  of  the  pleasure  lost  by  being  unable 
to  masticate  and  enjoy  the  food  for  a  large  portion 
of  life,  all  due  to  this  now  preventable  and  curable 
disease! 

SALIVARY  CALCULUS 

What  is  called  salivary  calculus  and  thought  to 
be  due  to  the  precipitation  of  calcareous  material 
from  the  saliva  is  in  fact  due  to  pyorrhea.  It  is 
now  generally  thought  to  be  the  cause  of  pyorrhea, 
in  some  cases  at  least,  but  we  feel  certain  that  it 
will  be  found  to  be  the  result,  rather  than  the 
cause,  of  pyorrhea.  We  have  not  had  the  oppor- 
tunity up  to  this  time  to  investigate  the  subject 
extensively,  and  the  literature  on  the  subject  that 


70  ALVEOLODENTAL  PYORRHEA 

has  been  available  to  us  is  worse  than  useless. 
Many  explanations  of  the  cause  of  the  condition 
are  absurd. 

Pus  discharging  from  a  pyorrhea  lesion  (even  a 
small  one)  flows  along  by  the  side  of  the  tooth,  and 
especially  in  the  ditch  between  two  teeth.  It  is 
held  and  made  to  flow  against  the  tooth  more 
completely  in  certain  locations  by  the  lips,  tongue, 
or  cheek  than  in  others,  but  it  is  sufl^icient  in  some 
cases  to  insure  calculus  formation  around  any 
tooth  involved.  As  the  pus  mixes  with  the  saliva 
in  certain  individuals  calcium  salts  are  thrown  out 
of  solution  and  are  deposited  on  the  tooth.  This 
continues  to  accumulate  until,  finally,  a  pretty 
heavy  deposit  of  yellowish  calculus  is  formed  on 
the  tooth  or  teeth.  It  is  heaviest  just  above  the 
edge  of  the  gum,  because  more  pus  passes  over 
that  location  than  further  from  the  lesion.  As 
the  discharge  passes  further  from  the  lesion  it  has 
lost  a  part  of  the  precipitable  matter  and  it  is 
diluted  more.  Therefore  the  calculus  formed  is 
thinner  the  further  from  its  source  we  go.  On 
account  of  the  fact  that  the  pus  is  caused  to  flow 
along  the  channel  where  two  teeth  stand  side  by 
side,  in  greatest  quantity,  the  calculus  is  thicker 
on  the  edges  of  the  teeth,  as  a  rule. 


MORBID  PROCESS  71 

SERUMAL  CALCULUS 

Not  only  may  certain  salts  in  pus  of  certain 
individuals  be  thrown  out  of  solution  and  thus 
form  calculi  on  the  enamel  of  the  teeth,  but  cer- 
tain substances  down  in  the  pyorrhea  pocket  (bac- 
teria and  their  products)  in  certain  individuals 
cause  precipitation  and  formation  of  calculi  on  the 
root  of  the  tooth  and  deep  in  the  lesion.  This 
is  "serumal"  calculus,  and  is  probably  a  source 
of  considerable  irritation  in  pyorrhea  lesions  wher- 
ever it  exists. 

CHANGE  OF  POSITION  OF  THE  TEETH  FROM  PYORRHEA 

One  of  the  things  formerly  thought  to  be  the 
cause  of  pyorrhea  is  malocclusion.  Many  an 
unfortunate  victim  has  had  his  or  her  teeth 
ground  off  by  the  dentist  as  a  remedy  for  pyorrhea, 
exposing  sensitive  dentin  for  the  balance  of  the 
life  of  the  tooth.  Instead  of  malocclusion  being 
the  cause  of  pyorrhea,  pvorrhea  is  the  cause  of 
much  of  the  malocclusion  seen. 

The  teeth  are  held  in  place  by  tough  fibers 
which  run  from  the  wall  of  the  alveolus  to  the 
cementum  of  the  tooth.  Whenever  these  fibers, 
the  peridental  membrane,  are  destroyed  on  one 
side  of  a  tooth  and  remain  intact  on  the  other  side, 
the  tooth  is  drawn  to  the  side  on  which  the  peri- 


72  ALVEOLODENTAL  PYORRHEA 

dental  membrane  is  still  living.  Sometimes  the 
peridental  membrane  is  destroyed  in  such  a  way 
that  the  tooth  is  twisted  in  its  socket  by  the  oppo- 
site fibers.  Teeth  are  sometimes  turned  almost 
one-fourth  around  in  this  way.  It  often  occurs 
that  the  incisors  pitch  forward  because  the  peri- 
dental membrane  is  destroyed  on  the  lingual  side. 
Strain  on  the  teeth,  such  as  biting  them  together 
or  biting  food,  gradually  increases  the  tilting. 
Tilting  is  also  encouraged  or  favored  by  the  swell- 
ing of  the  inflamed  tissue  on  the  diseased  side. 

The  fibers  of  the  peridental  membrane  are 
directed  both  apically  and  occlusally  from  their 
attachment  to  the  alveolar  wall.  The  tooth  is  held 
down  in  its  socket  by  those  directed  occlusally,  most 
of  which  are  located  at  the  border  of  the  alveolar 
process.  Whenever  the  peridental  membrane  all 
around  a  tooth  is  destroyed  to  below  the  original 
border  of  the  alveolar  process,  the  chief  fibers  that 
hold  it  down  are  gone.  The  swelling  of  the  soft 
tissue  produced  by  the  inflammation  as  the  dis- 
ease progresses  now  tends  to  crowd  or  force  the 
tooth  from  the  socket.  If  the  tooth  strikes  its 
opposite  fellow,  it  is  held  down  in  the  socket,  but 
if  it  does  not  rest  against  another  tooth,  it  grad- 
ually rises  out  of  the  socket  and  stands  higher 
than  the  other  teeth.  It  may  be  remarked  here 
that  such  a  tooth  can  be  forced  back  in  place  and 


MORBID  PROCESS  73 

retained  by  proper  mechanical  means  after  the 
disease  is  stopped. 

LOSS  OF  THE  ALVEOLAR  PROCESS 

Whenever  teeth  are  lost  from  any  cause  the 
alveolar  process  is  absorbed  or  removed  in  the 
course  of  several  months  or  years,  leaving  the 
maxillae  narrow  and  quite  different  in  appearance 
from  their  appearance  before  the  teeth  were 
removed  (Fig.  25). 

Pyorrhea  as  a  Source  of  Other  Systemic  Dis- 
eases— Septicemia,  Endocarditis,  Rheumatism. — 
The  opinion  is  held  by  quite  a  good  portion  of  the 
medical  profession  that  pyorrhea  is  the  source  of 
various  systemic  diseases.  We  are  not  prepared 
to  express  an  opinion  one  way  or  the  other.  It 
must  be  confessed  that  it  is  not  proved  to  be  so, 
however  much  we  may  believe  it.  The  fact  that 
a  patient  who  is  suffering  with  one  of  these  systemic 
diseases  also  has  pyorrhea  is  not  sufficient  evi- 
dence that  there  exists  any  etiologic  relation 
whatever  between  them,  because  practically  all 
other  grown  people  who  have  not  such  systemic 
disease  have  pyorrhea  also.  On  the  other  hand,  it 
would  seem  that  the  chances  of  pathogenic  bac- 
teria reaching  the  blood  through  pyorrhea  lesions 
are  great.  Most  pyorrhea  pockets  contain  one 
or  more  species  of  pathogenic  bacteria,  staphylo- 


74  ALVEOLODENTAL  PYORRHEA 

cocci,  streptococci,  pneumococci,  diplococci,  etc. 
The  endamebae  are  moving  about  among  the  bac- 
teria and  carrying  them  into  the  granulation  tissue 
among  the  granulations.  They  plant  and  replant 
the  bacteria  where  they  are  likely  to  gain  entrance 
into  the  blood-stream.  It  will  be  remembered 
that  granulations  consist  of  loops  of  blood-vessels, 
as  it  were,  with  very  thin,  permeable  walls.  This 
phase  of  the  subject  is  one  for  future  investigation. 


Infancy 


Childhood 


Maturity 


Senility 

Fig.  25. — Similar  pictures  to  these  are  common  in  text-books  on  anatomy 
and  physiology,  which  show  the  usual  changes  in  the  mandible  produced  by 
age.  The  loss  of  teeth  and  disappearance  of  the  alveolar  process  are  looked 
upon  as  physiologic  processes  because  they  occur  in  practically  all  people  if 
they  live  long  enough.  Instead  of  being  a  physiologic  change,  it  is  due  to 
alveolodental  pyorrhea,  and  in  the  light  of  our  present  knowledge  is  pre- 
ventable. 

75 


76  ALVEOLODENTAL  PYORRHEA 

SUMMARY 

A  tooth  is  held  in  its  bony  socket  by  a  tough 
peridental  membrane  which  consists  largely  of 
fibers  attached  to  the  alveolar  wall  and  to  the 
cementum  of  the  tooth. 

Alveolodental  pyorrhea  begins  in  a  lesion  pro- 
duced by  damage  to  the  edge  (tearing  loose)  of  the 
peridental  membrane.  Such  lesions  may  be  pre- 
vented from  healing  until  they  chance  to  become 
infected  by  endamebae,  by  food  particles  forced 
into  them  from  time  to  time. 

Once  endamebae  are  inoculated  into  such  a 
lesion,  they  prevent  healing  and  cause  the  lesion 
to  extend  slowly  but  surely.  The  peridental  mem- 
brane is  slowly  destroyed,  leaving  the  alveolar 
wall  and  tooth  bare.  Large  quantities  of  pus  are 
formed. 

As  the  peridental  membrane  attaching  the 
alveolar  wall  to  the  tooth  is  destroyed,  the  bone, 
which  no  longer  can  perform  the  function  for  which 
it  was  intended, — supporting  the  tooth, — is  slowly 
absorbed  or  removed. 

It  is  not  known  whether  the  endamebae  damage 
or  attack  the  tissue  directly.  They  probably  do 
their  damage  by  crawling  about  among  the  gran- 
ulation tissue  in  search  of  certain  nuclear  bodies 
or  cells  for  food,  and  incidentally  planting  and  re- 
planting bacteria  among  the  granulations.  The  bac- 


MORBID  PROCESS  77 

teria  could  not  invade  the  tissue  unaided  by  the 
endamebae.  Different  bacterial  flora  in  the  mouth 
of  different  individuals  is  one  of  the  influences 
which  leads  to  great  variation  in  the  character 
and  progress  of  the  disease  in  different  individuals. 

Whenever  the  destructive  process  has  advanced 
far  enough  and  the  supporting  structures  have 
been  destroyed  suflRciently,  the  tooth  gets  loose  in 
its  socket.  Finally,  whenever  there  no  longer 
remains  sufl[icient  tissue  to  support  it,  it  either 
falls  out  or  is  removed. 

One  lesion  infected  is  a  constant  source  of  infec- 
tion to  any  other  favorable  soil  that  may  be  pre- 
pared by  damage  or  trauma  that  may  occur  to  the 
peridental  membrane.  Sooner  or  later  the  sup- 
porting structures  of  all  the  teeth  are  involved. 
After  months  and  years  of  suppuration  one  tooth 
after  another  is  lost,  until  finally  all  are  gone. 

The  amount  of  blood  lost  during  the  active 
early  stage  of  the  disease  is  estimated  to  be  at 
least  a  gallon  a  year.  This  may  be  harmful.  The 
amount  of  pus  produced  during  the  time  required 
for  all  the  teeth  to  be  removed  by  this  disease  is 
estimated  to  be  at  least  eight  gallons.  This  may 
also  have  an  influence  on  the  health  and  possibly 
on  the  longevity  of  the  individual. 

It  is  also  quite  probable  that  pyorrhea  lesions 
may  be  the  portal  of  entry  of  pathogenic  bacteria 
into  the  blood-stream  as  well  as  bacterial  poisons. 


CHAPTER  V 
CONTAGIOUSNESS 

Before  we  knew  the  specific  cause  of  alveolo- 
dental  pyorrhea  and  how  to  diagnose  the  disease 
certainly  in  all  stages,  it  was  impossible  to  know 
whether  or  not  it  was  contagious.  The  length  of 
time  necessary  for  the  disease  to  develop  to  a 
stage  where  it  is  recognized  by  the  patient  and 
likely  to  be  diagnosed  by  the  dentist  or  physician 
is  so  great  that,  naturally,  the  source  of  infection 
is  never  thought  of.  No  doubt  in  most  all  cases 
several  years  intervene — in  certain  cases  even 
twenty  or  more  years — between  the  date  of  primary 
infection  and  recognition  of  the  disease. 

Another  factor  which  would  lead  to  difficulty 
in  determining  the  contagiousness  of  the  disease 
is  its  many  sources.  Practically  all  adults  have 
the  infection,  and  may,  therefore,  be  sources  of 
infection  to  others.  In  the  presence  of  such  a 
condition  it  would  be  impossible  to  trace  the  infec- 
tion in  a  given  case  to  its  source.  It  is  quite  true 
that  many  have  thought  the  disease  contagious  or 
infectious  in  some  way.  The  common  observa- 
tion  of  its   much   greater   prevalence   in   certain 

78 


CONTAGIOUSNESS  79 

families  than  in  others  is  an  indication,  but  not 
proof,  of  contagiousness  or  infectiousness.  It 
resembles  other  contagious  diseases — measles, 
smallpox,  tuberculosis,  etc. — in  this  respect.  In 
regard  to  any  disease  due  to  specific  infection  there 
is  greater  tendency  for  it  to  occur  in  households 
and  communities  in  which  other  cases  exist  or 
have  existed. 

Now  that  we  know  the  specific  causative  agent 
in  pyorrhea,  Endamoeba  buccalis,  we  can  under- 
stand the  greater  prevalence  in  certain  families 
and  groups  of  people  who  are  closely  associated. 
Let  us  suppose  a  husband  has  the  disease.  Close 
association  with  his  wife,  eating  and  drinking 
after  each  other,  kissing,  etc.,  expose  her  especially 
to  the  infection,  which  she  sooner  or  later  surely 
gets.  Finally,  whenever  their  children  grow  up 
and  get  old  enough  to  become  infected,  they  could 
hardly  escape  on  account  of  the  constancy  and 
favorability  of  the  source  of  infection  to  which 
they  are  exposed.  A  child  might  be  taught  early 
not  to  eat  or  drink  after  others  than  their  im- 
mediate families,  but  in  what  home  is  the  individual 
drinking-cup  to  be  found.?  Where  the  father  and 
mother  are  in  the  most  advanced  and  infectious 
stage,  nothing  short  of  individual  drinking-cups 
and  other  precautions  could  promise  to  protect 
the  children  who  are  growing  up.     The  common 


8o  ALVEOLODENTAL  PYORRHEA 

drinking-cup  in  public  places,  stores  and  shops, 
parks,  factories,  etc.,  must  be  a  great  source  of 
infection.  Such  a  cup  must  have  endamebae  on 
it  almost  all  the  time. 

We  are  often  asked  whether  we  think  the  disease 
is  "catching."  To  this  we  reply  there  is  not  the 
slightest  known  evidence  that  Endamceba  buccalis 
lives  and  reproduces  anywhere  in  the  world  except 
in  the  mouth  and  adjacent  structures  of  man  and 
perhaps  certain  animals,  and  since  this  parasite 
is  the  essential  cause  of  pyorrhea,  it  is  caught  from 
some  other  person  in  every  case.  Everybody  who 
has  pyorrhea  got  it  from  somebody  else,  usually, 
if  not  always,  by  putting  more  or  less  saliva  and 
pus  from  the  other  person's  mouth  into  his  own 
mouth.  It  is  not  necessary  that  the  quantity 
be  large  enough  to  be  seen  on  ordinary  observa- 
tion to  be  sufficient  to  infect.  Microscopic 
quantities  may  contain  many  endamebae.  One 
should  be  sufficient  to  start  the  disease  if  planted 
in  favorable  soil. 

The  spread  of  pyorrhea  would  soon  be  checked 
materially  if  the  facts  that  we  now  know  about 
the  disease  could  be  brought  clearly  to  the  atten- 
tion of  the  public.  If  the  real  facts  were  known, 
the  pernicious  habits  of  drinking  and  eating  after 
each  other,  putting  things  of  unknown  cleanliness 


CONTAGIOUSNESS  8i 

in  the  mouth,  kissing  in  the  mouth,  etc.,  would  be 
rapidly  reduced,  at  least. 

Another  factor  that  may  some  day  contribute 
to  reduction  in  the  incidence  of  the  disease  is  the 
cure  of  cases  or  reduction  in  the  number  of  cases. 
Every  case  cured  is  just  one  less  source  of  infection. 
Not  only  that,  such  an  individual  will  usually  be  a 
kind  of  educator  for  others,  for  no  one  is  likely  to 
be  cured  and  remain  cured  without  learning,  during 
his  treatment,  some  of  the  fundamental  lessons 
about  the  disease.  Now  that  the  disease  is  cur- 
able and  its  return  preventable,  there  should  be 
an  ever-increasing  number  of  cured  persons.  In 
addition,  other  younger  people  will  avoid  infec- 
tion, and  in  time  the  proportion  of  the  population 
of  the  community  who  have  the  disease  should 
get  less  than  it  is  at  present. 

SUMMARY 

Endamceba  buccalis,  the  specific  cause  of  pyor- 
rhea, is  not  known  to  live  and  reproduce  anywhere 
in  the  world  except  in  the  mouth  and  adjacent 
structures  of  man.  It  is  "caught,"  either  directly 
or  indirectly,  from  another  person  who  has  pyor- 
rhea by  putting  more  or  less  saliva  and  pus-con- 
taining endamebae  from  the  infected  person's 
mouth  into  the  mouth  of  the  one  who  becomes 
infected. 

6 


CHAPTER  VI 

SYMPTOMATOLOGY 

The  symptoms  of  alveolodental  pyorrhea  vary 
with  the  stage  of  the  disease,  the  bacterial  flora 
in  the  mouth,  including  probably  the  spirochetes, 
the  oral  hygiene  practised  by  the  patient,  the 
teeth  involved,  and  individual  influences,  as  well 
perhaps  as  other  factors  that  we  do  not  under- 
stand at  this  time.  It  should  be  clearly  under- 
stood that  the  disease  is  one  of  many  years'  dura- 
tion, and  that  different  teeth  are  usually  found 
to  be  in  different  stages  at  the  same  time.  In  the 
same  patient  one  or  more  teeth  may  be  found 
very  loose  and  in  the  very  last  stage ;  one  or  more 
others  may  be  in  an  advanced  stage,  but  still 
firmly  held  in  their  sockets;  one  or  more  others 
may  be  in  a  less  advanced  stage,  but  have  the 
disease  well  established;  one  or  more  others  may 
be  in  the  earliest  stage,  in  which  careful  micro- 
scopic examination  may  be  required  to  demon- 
strate the  pus  and  endamebae  which  can  be  ob- 
tained by  carefully  removing  material  from  beneath 
the   collar  of  gum,   especially  that   between   the 

teeth;   and  still  one  or  more  other  teeth  and  their 

82 


SYMPTOMATOLOGY  83 

peridental  membrane  may  be  perfectly  normal  all 
in  the  same  mouth. 


BLEEDING  FRQM  GUMS  THE  EARLIEST  SYMPTOM 

Bleeding  from  the  gums  is  probably  the  earliest 
symptom  recognized  by  the  patient.  This  comes 
on  so  insidiously  and  is  supposed  to  be  such  a 
harmless  thing  that  little  attention  is  paid  to  it. 
It  occurs  in  almost  all  cases,  but  is  very  variable 
in  amount  with  different  individuals.  Picking 
the  teeth  may  be  followed  by  the  flow  of  a  little 
blood.  The  patient  thinks  he  wounded  the  gum 
and  pays  it  little  attention.  Sucking  the  teeth 
may  cause  a  little  bleeding  of  the  gum  around 
one  or  more  teeth.  Brushing  the  teeth  may  be 
followed  by  the  flow  of  a  little  blood.  Perhaps 
only  enough  blood  to  color  the  first  spit  or  two  of 
saliva  is  all  that  is  noticed.  In  other  instances 
when  early  lesions  exist  several  drops  of  blood  may 
be  expectorated.  We  have  seen  a  few  patients 
whose  gums  would  occasionally  break  loose  and 
bleed  apparently  without  any  provocation.  The 
blood  comes  from  the  granulation  tissue  which 
makes  one  side  of  the  lesion  or  pocket.  Granula- 
tion tissue  generally  bleeds  freely  upon  the  slight- 
est manipulation.  The  tissue  that  bleeds  is  chiefly 
between  the  teeth.  Chewing  food  causes  bleed- 
ing when  one  has  pyorrhea,  especially  in  the  early 


84  ALVEOLODENTAL  PYORRHEA 

stage,  but  the  blood  is  promptly  diluted  with  the 
food  and  not  tasted.  The  quantity  of  blood  that 
oozes  from  the  gums  and  is  swallowed  during  a 
meal  in  some  cases  must  be  considerable — several 
drops,  at  least,  in  many  cases.  There  is  less  bleed- 
ing in  far-advanced  cases,  as  a  rule. 

SORENESS  OF  THE  GUMS  AND  OF  THE  TEETH  ON  PRESSURE 

There  is  often  a  slight,  sometimes  considerable, 
soreness  or  unnatural  feeling  of  the  diseased  gum 
from  time  to  time,  but  the  patient  usually  mis- 
takes it  for  a  little  something  that  has  lodged 
between  the  teeth  and  is  pressing  against  the  gum, 
or  a  little  injury  that  has  occurred  in  some  way. 
In  fact,  the  slight  unnatural  feeling  is  not  seriously 
thought  of  by  the  patient,  and  usually  passes  away 
in  a  day  or  two,  to  recur  in  a  few  days.  After 
the  disease  advances  far  enough,  pressure  on  the 
tooth,  as  by  biting  the  teeth  together  or  eating, 
elicits  soreness.  Sometimes  this  is  considerable 
and  gives  rise  to  more  or  less  continued  discomfort 
for  days  or  weeks  at  a  time.  Probably  this  is 
brought  about  by  food-particles  being  carried  into 
the  lesions.  Other  patients  suffer  very  little  pain 
or  discomfort  during  the  many  years  the  disease 
lasts. 


SYMPTOMATOLOGY  85 

BAD  TASTE  IN  THE  MOUTH 

During  the  early  stage  of  the  disease,  if  only  one 
or  two  teeth  are  involved,  perhaps  there  is  not 
enough  pus  formed  or  decomposition  in  the  pockets 
to  be  very  noticeable  to  the  patient.  As  the  disease 
advances  more  pus  is  produced,  there  is  more  dead 
or  dying  tissue  in  the  lesion,  and  there  is  more 
decomposition  of  food  and  pus  in  the  larger  pock- 
ets. This  gives  rise  to  a  bad  taste  in  the  mouth, 
especially  after  the  patient  has  been  asleep  and 
quiet  for  a  few  hours.  During  the  waking  hours 
the  pus  and  decomposing  material  are  swallowed 
or  spit  out  every  few  minutes  and  therefore  not 
allowed  to  accumulate.  On  the  other  hand,  dur- 
ing sleep  they  accumulate  and  upon  waking  they 
are  in  sufficient  quantity  to  give  rise  to  a  bad  taste 
in  the  mouth. 

FOUL  BREATH 

This  pus  and  sloughing,  decomposing  material 
usually  have  a  very  bad  odor.  At  first  it  is  so  little 
as  to  be  unnoticed,  except  perhaps  after  several 
hours  of  sleep  and  quiet.  As  the  quantity  gets 
larger  an  offensive  breath  is  present,  noticeable 
at  all  times  to  others,  and  after  a  little  accumula- 
tion, to  the  patient  himself.  The  odor,  no  doubt, 
is  produced  in  most  instances  by  spirochetes  in  the 


86  ALVEOLODENTAL  PYORRHEA 

lesion,  but  in  some  the  characteristic  fecal  odor 
strongly  suggests  that  produced  by  the  colon 
bacillus.  In  other  cases  the  odor  is  the  sickening, 
raw  flesh  odor  produced  no  doubt  by  profuse  flow 
of  pus. 

PYORRHEA 

Pyorrhoea  is  present  during  all  stages  of  the 
disease,  but  the  quantity  of  pus  is  not  large 
enough  to  be  recognized  macroscopically  until  it 
has  existed  for  a  considerable  length  of  time.  The 
amount  of  pus  produced  by  lesions  of  equal  size 
in  difi^erent  people  varies  considerably.  Perhaps 
the  secondary  pyogenic  infection  and  individual 
idiosyncrasy  are  largely  the  cause.  When  only 
the  posterior  teeth  are  involved,  the  patient  does 
not  notice  the  pyorrhea.  Whenever  the  front 
teeth  are  suflBciently  diseased,  pus  may  be  noticed 
oozing  from  around  the  teeth.  Properly  applied 
pressure  squeezes  out  sometimes  a  drop  or  more 
of  thick,  creamy  pus.  We  have  seen  many  pa- 
tients who  had  learned  to  massage  the  pus  out  of 
their  pyorrhea  pockets.  Pressing  against  the 
end  of  the  tooth  often  will  cause  pus  to  appear  at 
the  edge  of  the  pocket.  So  also  will  pushing  the 
tooth  from  side  to  side.  The  manipulation  in 
either  case  simply  forces  the  pus  out  of  the  pocket. 


SYMPTOMATOLOGY  87 

SENSITIVENESS  OF  THE  NECK  OF  THE  TOOTH 

After  the  disease  has  existed  for  a  time  the  peri- 
dental membrane  which  normally  covers  the  neck 
and  the  root  of  the  tooth  is  slowly  but  surely 
destroyed,  leaving  that  part  of  the  tooth  exposed. 
In  certain  individuals  the  dentin  is  especially 
sensitive  to  heat  and  cold,  sweet  and  sour,  etc. 
This  symptom  is  present  to  some  extent  in  all 
advanced  cases,  but  varies  greatly  in  different 
cases.  It  is  quite  noticeable  in  some  early  cases, 
even  before  retraction  has  occurred. 

RETRACTION 

Retraction  of  the  gums  is  not  an  early  symptom, 
except  in  those  cases  where  it  has  been  produced 
by  overuse  of  the  tooth-brush  and  powders  and 
pastes  containing  powders.  As  the  alveolar  proc- 
ess is  absorbed  the  gum  retracts,  the  tooth  appear- 
ing larger  and  longer.  In  some  cases  the  tooth 
gets  loose  and  is  lost  before  the  alveolar  bone  is 
absorbed,  and  in  such  cases  there  is  not  much 
retraction.  In  others,  perhaps  the  less  rapidly 
progressing  cases,  the  bone  is  absorbed  and  re- 
traction of  the  gum  occurs,  until  sometimes  the 
length  of  the  part  of  the  tooth  that  is  uncovered 
by  gum  is  more  than  twice  as  great  as  normal. 


88  ALVEOLODENTAL  PYORRHEA 

LOOSENESS  OF  THE  TEETH 

The  teeth  get  loose  sooner  or  later  in  all  cases 
if  pyorrhea  is  allowed  to  run  its  course,  because 
it  always  causes  the  loss  of  the  teeth.  For  a  time 
the  tooth  will  get  very  loose  and  then  tighten  up 


Fig.  26. — A  case  of  pyorrhea  involving  all  the  teeth.     The  gums  were  mas- 
saged to  bring  out  the  pus,  which  can  be  seen  at  the  gum  margins. 

again.  Sometimes  months  or  years  before  it  is 
finally  lost  it  may  be  quite  loose.  The  least  force 
moves  it  from  side  to  side.  The  patient  can  move 
it  aside  with  his  tongue.  In  addition  to  this 
loosening,  due  to  destruction  of  the  tissues  which 


SYMPTOMATOLOGY  89 

normally  hold  the  teeth  firm,  there  also  sometimes 
occurs  sufficient  thickening  of  the  peridental  mem- 
brane to  lift  the  tooth  from  its  bed  in  the  socket, 
in  which  instance  the  tooth  gives  considerably 
when  force  is  applied  to  it. 

CHANGES  IN  THE  POSITION  OF  TEETH— MALOCCLUSION 

Inflammation  of  the  peridental  membrane  causes 
more  or  less  swelling  or  hyperplasia  of  the  tissue. 
This  tends  to  lift  the  tooth  from  the  socket, 
especially  when  no  opposing  pressure  is  exerted  to 
prevent  it.  When  one  of  two  teeth  that  normally 
articulate  with  each  other  is  lost  for  any  cause,  the 
other  is  not  kept  pressed  in  place,  and  if  diseased 
with  pyorrhea,  is  forced  outward  from  the  bottom 
of  the  socket  by  the  thickened  peridental  membrane. 
The  incisors  normally  do  not  articulate  in  the 
majority  of  people,  and  therefore  are  especially 
likely  to  present  this  symptom  of  pyorrhea.  The 
tooth  may  be  noticed  to  be  elongating.  This  is 
often  the  first  symptom  that  attracts  attention. 
It  often  occurs  that  the  pyorrhea  lesion  is  much 
more  extensive  on  one  side  of  a  tooth  than  on  an- 
other. In  such  an  instance  the  thickening  of  the 
peridental  membrane  exerts  constant  pressure  in 
the  opposite  direction,  causing  the  structures  to 
give  way  gradually  and  thus  the  tooth  is  moved 
sideways.     The  space  between  the  teeth  widens. 


90  ALVEOLODENTAL  PYORRHEA 

More  frequently  there  is  combined  action,  lifting 
the  tooth  in  the  socket  and  tilting  in  one  direction 
or  another.     Teeth  may  be  lifted  and  tilted  to  one 


Fig.  27. — The  teeth  of  some  people  seen  .  j  be  more  firmly  set  than  others. 
This  is  one  of  them.  There  is  no  moving  of  the  teeth  in  spite  of  a  bad  pyor- 
rhea. The  interdental  soft  tissue  has  been  destroyed.  There  is  no  soft  tissue 
connection  between  the  labial  and  lingual  gums. 

side  or  the  other.  Often  they  are  tilted  forward, 
giving  rise  to  increased  prominence  of  the  front 
teeth.  Sometimes  considera|»lt  twisting  of  a  tooth 
from  its  normal  position  may  be  caused  in  this 


SYMPTOMATOLOGY 


91 


way.     It  is  remarkable  that  so  much  change  in  the 
position  of  the  teeth  can  be  produced  with  so  Httle 


Fig.  28. — Bad  pyorrhea  in  a  young  woman.  There  are  deep  pyorrhea 
pockets  around  each  of  the  teeth,  and  some  of  them  have  been  moved  re- 
cently from  their  normal  positions.  The  endamebae  disappeared  from  the 
oral  administration  of  ipecac.     No  emetin  was  given  hypodermatically. 

and  often  no  pain  whatsoever.     No  doubt  it  is  due 
largely  to  the  slowness  of  the  process.     The  action 


92 


ALVEOLODENTAL  PYORRHEA 


is  so  slow  that  the  tooth  often  remains  fairly  firmly 
held  for  several  years. 


•  ■«^.  <m,»i>m 


Fig.  29. — Rapidly  progressing  case  of  pyorrhea  in  a  young  woman.  Note 
retraction  of  gum  from  canine  tooth,  and  how  other  teeth  have  moved  out  of 
their  normal  position — the  extent  to  which  two  of  the  teeth  have  risen  out  of 
their  socket.  The  endamebae  disappeared  from  this  case  after  three  daily 
hypodermics  of  one-half  grain  of  emetin  each. 

The  molar  teeth  are  often  tilted  in  one  direction 
or  another  in  the  line  of  least  resistance  whenever 


SYMPTOMATOLOGY  93 

they  are  lifted  in  their  socket  by  thickened  peri- 
dental membrane.  When  one  has  been  lost,  and 
the  absorption  of  the  alveolar  bone  makes  quite 
a  gap,  the  tooth  behind  it  tilts  forward  and  some- 
times almost  lies  down  in  the  gap  before  it  is  finally 
lost  from  the  pyorrhea.  Changes  in  the  position 
of  the  teeth  of  an  adult  may,  therefore,  be  con- 
sidered a  most  significant  symptom  of  pyorrhea. 

GUM-BOILS 

Gum-boils  may  sometimes  occur  without  pyor- 
rhea being  present.  Infection  extending  down  a 
root-canal  and  escaping  into  the  peridental  soft 
tissue  may  produce  abscesses.  Most  of  them  are 
produced  by  poorly  drained  pyorrhea  pockets 
getting  stopped  up  in  some  way  or  another.  For- 
eign substances,  like  food  particles,  forced  into 
them  may  interfere  with  their  drainage  and  cause 
an  abscess. 

CHANGES  IN  THE  GUMS 

Retraction  of  the  gums  has  already  been  men- 
tioned as  a  symptom  of  pyorrhea  of  long  standing. 
In  the  early  stage  there  occur  more  or  less  redness 
and  slight  swelling  of  the  edge  of  the  gum.  This 
may  be  so  slight  as  not  to  be  noticeable,  especially 
in  the  interdental  gum.  Usually,  however,  the 
interdental    papilla    extend    a    little   higher   than 


94  ALVEOLODENTAL  PYORRHEA 

normal  and  more  or  less  edema  is  present.  Red- 
ness is  not  so  marked  as  in  the  gum  in  front  of  or 
behind  the  tooth.  Often,  in  spite  of  very  deep 
pockets  beside  a  tooth,  there  is  little  or  no  redness. 


Fig.  30. — ^The  last  stage  of  pyorrhea.  Note  the  pus  on  teeth.  This  was 
brought  out  by  massaging  the  gum  just  before  the  picture  was  taken.  Note 
that  lower  teeth  have  fallen  over  because  of  the  loss  of  the  supporting  struc- 
tures. Such  teeth  are  held  by  only  a  very  little  bit  of  living  tissue  at  the  bot- 
tom of  the  socket. 


In  fact,  the  gum  may  appear  to  be  attached  to  the 
tooth  in  the  normal  manner  until  it  is  examined 
carefully,  when  it  is  found  that  a  suitable  narrow 
instrument  can  be  passed  down  by  the  side  of  the 


SYMPTOMATOLOGY 


95 


tooth  for  a  considerable  distance  without  meeting 
with  resistance.  If  the  instrument  is  then  manipu- 
lated, a  little  blood  wells  out  of  the  pocket. 

After  the  disease  is  advanced  often  there  is  a 
red  or  purple  appearance  of  the  gum  over  the 


Fig.  3 1 . — The  last  stage  of  the  disease.  Imagine  what  a  fruitful  source  of 
infection  such  an  individual  may  be  to  others!  Such  teeth  pain  or  worry 
him.  He  picks  at  them  unconsciously  with  his  fingers,  and  is  likely  then  to 
handle  things  handled  by  others. 

tooth,  and  extending  perhaps  as  far  as  the  level 
of  the  apex  of  the  root  of  the  tooth.  We  think  in 
most  cases  of  this  kind  there  has  also  been  consider- 
able destruction  of  the  periosteum  covering  the  al- 
veolar bone  over  the  tooth,  as  well  as  that  lining 


96 


ALVEOLODENTAL  PYORRHEA 


the  socket.  Though  the  absence  of  redness  and  in- 
flammation of  the  gum  cannot  be  depended  upon 
to  exclude  pyorrhea,  its  presence  is  a  symptom  of 
great  diagnostic  value.     It  is  true  that  inflamma- 


Fig.  32. — The  last  stage  of  pyorrhea. 

tion  may  be  produced  by  trauma  or  certain  other 
things,  but  it  is  usually  temporary. 


ABSORPTION  OF  ALVEOLAR  BONE 

Absorption  of  alveolar  bone  begins  as  soon  as 
any  part  of  the  peridental  membrane  between  it 
and  the  tooth  is  destroyed,  but  it  is  usually  many 


SYMPTOMATOLOGY  97 

months  or  years  before  there  has  been  sufficient 
absorption  for  this  to  become  a  prominent  symp- 
tom. The  absorption  continues  after  the  tooth  is 
lost  until  the  alveolar  process  has  been  entirely 
removed.  This  may,  therefore,  be  more  correctly 
considered  as  a  symptom  or  evidence  of  the  previ- 
ous existence  of  pyorrhea,  instead  of  its  presence. 

SUMMARY 

The  symptoms  of  alveolodental  pyorrhea  are 
variable  in  different  individuals. 

The  earliest  symptom  usually  is  bleeding  from 
one  or  more  gums.  It  may  be  produced  by  the 
least  manipulation  or  force,  like  brushing  the 
teeth,  picking  the  teeth,  sucking  air  between  them, 
etc. 

Soreness  and  unpleasant  feeling  of  the  gums  and 
of  the  teeth  on  pressure  may  be  present  for  a  long 
time.  Often  in  the  last  stage,  there  is  considerable 
soreness  at  times. 

Bad  taste  in  the  mouth,  especially  in  the  morn- 
ing, is  present  in  most  cases,  but  usually  it  comes 
on  so  insidiously  and  has  existed  so  long  that  the 
patient  simply  accepts  it  as  a  natural  condition. 
He  is  more  impressed  with  it  whenever  he  gets 
rid  of  it  from  appropriate  treatment.  The  relief 
attracts  his  attention. 

Foul  breath  is  a  symptom  in  all  advanced  cases. 
7 


98  ALVEOLODENTAL  PYORRHEA 

It  varies  with  the  bacterial  and  spirochetal  flora 
in  the  individual's  mouth. 

Pyorrhea  is  a  constant  symptom.  Pus  can 
always  be  demonstrated  by  competent  micro- 
scopic examination,  but  in  the  advanced  stage 
macroscopic  pus  can  be  demonstrated. 

Sensitive  dentin  is  often  exposed  by  retraction 
of  the  gums. 

In  the  late  stage  of  the  disease,  involving  a 
given  tooth,  the  tooth  gets  loose  in  its  socket  and 
may  be  tilted  about  by  little  force. 

Malocclusion  occurs  especially  with  teeth  that 
do  not  articulate  with  or  press  against  others. 
Sometimes  they  rise  out  of  their  socket  one-eighth 
inch  or  more. 

Absorption  of  alveolar  bone  and  the  resulting 
retraction  of  the  gum  are  constant  symptoms  of  the 
late  stage  of  the  disease. 


CHAPTER  VII 
DIAGNOSIS 

Here,  as  in  most  other  diseases,  the  first  thing 
necessary  for  the  diagnosis  is  to  suspect  the  pres- 
ence of  the  disease.  On  account  of  the  great  prev- 
alence of  alveolodental  pyorrhea  one  may  feel 
practically  sure  of  its  existence,  to  some  extent,  at 
least,  in  almost  all  adults  and  in  a  large  percentage 
of  children.  Its  presence  should  be  suspected  in 
all  people  until  proved  otherwise. 

It  should  be  understood  that  pus  formation 
results  from  any  lesion  accompanied  by  a  break 
in  the  soft  tissues  of  the  mouth.  The  amount  of 
pus  may  be  great,  or  it  may  be  so  small  as  to  re- 
quire microscopic  examination  to  demonstrate  it. 
Unless  endamebae  are  present,  lesions  in  the  gums 
heal  rapidly  provided  the  cause  is  removed.  Dur- 
ing the  period  the  lesion  exists  there  is  more  or 
less  pus  formation.  Such,  however,  does  not 
constitute  the  specific  disease  discussed  in  this 
book. 

HISTORY 

The  history  given  by  the  patient  of  bleeding 
gums  for  a  considerable  time,  changing  in  the  posi- 

99 


ICX3 


ALVEOLODENTAL  PYORRHEA 


r 
y 

\ 


FJg-  33-  — Younger 
dental  scaler  No.  22, 
the  best  instrument 
with  which  to  obtain 
material  containing 
endamebx  from  most 
pyorrhea  lesions.  Its 
mate,  No.  23,  is  better 
suited  to  a  few  of  the 
lesions. 


tion  of  certain  teeth,  soreness  of  the 
teeth,  gum-boils,  looseness  of  the 
teeth,  and  finally  pus  discharging 
from  around  the  teeth  is  reasonably 
certain  to  mean  that  the  patient 
has  endamebic  pyorrhea.  Any  one 
or  all  of  these  symptoms  could  be 
caused  by  other  things,  but  if  so, 
the  cause  would  usually  be  appar- 
ent or  known. 

When  a  patient  is  examined  for 
pyorrhea  all  of  the  teeth  and  gums 
should  be  inspected  systematically, 
both  on  the  labial  and  on  the  lin- 
gual side.  By  inspection  inflamed, 
swollen  gums,  retracted  gums,  teeth 
out  of  position  without  being 
pushed  out  by  other  teeth,  and 
rather  wide  lesions  may  be  ob- 
served. 

Suitable  instruments  to  feel  for 
lesions  or  pockets  in  different  sus- 
pected places  are  very  valuable. 
An  ordinary  wooden  toothpick  will 
do  in  the  absence  of  something 
better,  but  the  most  convenient 
instrument  for  this  purpose  is  a 
Younger  dental  scaler  No.  22  (Fig. 


DIAGNOSIS  loi 

33).  The  mate  to  this,  No.  23,  is  often  useful  to 
reach  places  to  which  the  No.  22  is  not  adapted. 
With  this  little  instrument  the  presence  or  absence 
of  lesions  can  be  determined  by  gently  pressing  the 
point  of  this  instrument  down  by  the  side  of  a  tooth 
where  the  disease  appears  to  exist.  Frequently  it 
goes  very  deep  without  meeting  with  resistance — 
much  deeper  than  one  would  have  expected  from 
the  appearance.  This  is  especially  true  of  lesions 
between  the  teeth.  More  or  less  pus  is  brought 
out  by  scooping  with  the  flat  side  of  the  scaler. 
Frequently  there  may  be  sufficient  pus  present  to 
be  squeezed  out  either  by  massaging  the  gum  from 
the  level  of  the  end  of  the  root  of  the  tooth  toward 
the  crown  or  by  moving  the  tooth  from  side  to 
side.  The  pus  appears  between  the  margin  of  the 
gum  and  the  tooth.  Such  a  condition  justifies  a 
practical  diagnosis  of  pyorrhea  without  further  evi- 
dence. Loose  permanent  teeth  hardly  result  from 
any  other  condition  than  pyorrhea. 

MICROSCOPIC  EXAMINATION 

Endameba,  being  a  microscopic  parasite,  it 
would  not  be  possible  to  say  positively  that  any 
case  of  pyorrhea  had  endamebae  present  without 
making  a  microscopic  examination.  We  wish  to 
say  here,  however,  that  though  the  ideal  way  to 
make  the  diagnosis  is  by  microscopic  examination, 


I02  ALVEOLODENTAL  PYORRHEA 

diagnoses  sufficiently  reliable  for  practical  pur- 
poses can  be  made  without  it.  We  advise  all 
whom  circumstances  permit  to  make  or  confirm 
their  diagnoses  by  microscopic  examination. 

Method  of  Obtaining  Material  for  Examination. 
— In  obtaining  material  for  microscopic  examina- 
tion for  endamebae  the  fact  that  most  of  the  para- 
sites are  in  the  edge  of  the  peridental  membrane 
in  the  very  bottom  of  the  lesion  should  be  kept  in 
mind,  and  an  effort  should  be  made  to  scrape  the 
material  for  examination  from  the  bottom  of  the 
lesion.  Some  endamebae  can  usually  be  found  in 
the  pus  that  can  be  massaged  out  or  obtained  by 
working  the  tooth  back  and  forth,  but  not  as  many 
as  in  material  scraped  from  the  bottom.  With 
the  dental  scaler  or  other  instrument  one  should 
try  to  scrape  some  material  from  the  very  bottom 
of  the  lesion.  In  advanced  disease  much  pus  and 
other  material  is  obtained  also,  but  in  early  lesions 
often  a  very  small  amount  is  obtained.  Avoid 
causing  bleeding  as  much  as  possible.  Blood 
dilutes  the  material  too  much. 

Preparation  of  Stained  Specimens  for  Exam- 
ination.— Endamebae  can  be  demonstrated  either 
in  stained  preparations  or  in  unstained  wet  prepara- 
tions, in  which  case  the  living  endamebae  are  seen 
showing  their  characteristic  ameboid  motion. 

To   prepare   a   stained   specimen   the   material 


DIAGNOSIS  103 

obtained  from  the  lesion  is  spread  thinly  on  a 
glass  slide  and  stained.  There  are  many  methods 
of  staining,  each  having  certain  advantages,  per- 
haps, but  the  following  is  good  enough  for  all  ordi- 
nary purposes.  The  stains  used  are  among  those 
commonly  in  use  in  all  laboratories. 

1.  The  dried  film  is  fixed  with  heat  by  passing 
it  rapidly,  film  side  upward,  through  the  flame 
of  an  alcohol  lamp  or  Bunsen  burner  two  or  three 
times.  The  slide  should  not  get  so  hot  but  that 
it  can  be  touched  to  the  back  of  the  hand  without 
burning. 

2.  Cover  the  film  with  carbolfuchsin — one  or 
two  drops  are  all  that  is  necessary. 

3.  Wash  off  at  once  with  water.     (Do  not  dry.) 

4.  Cover  the  film  with  Loflfler's  solution  of 
methylene-blue.  One  or  two  drops  are  sufficient. 
Allow  to  stain  for  about  one-quarter  to  one-half 
minute. 

5.  Wash  off  with  water.  Dry  by  blotting  or  by 
simply  fanning  in  the  air  for  a  few  minutes. 

The  carbolfuchsin  stains  all  objects  on  the  slide 
— pus-cells,  bacteria,  etc.  It  is  a  quick,  strong 
stain.  Loffler's  methylene-blue  is  also  a  strong 
stain,  and  if  the  preparation  which  has  first  been 
stained  red  with  the  carbolfuchsin  should  be 
stained  with  the  methylene-blue  long  enough,  the 
red  would  be  entirely  displaced  by  the  blue  and 


I04  ALVEOLODENTAL  PYORRHEA 

everything  on  the  slide  would  be  stained  blue. 
The  red  is  displaced  by  the  blue  more  rapidly  in 
some  objects  on  the  slide  than  others,  and  in  cer- 
tain portions  of  a  given  cell  or  endameba  than 
others.  If  we  carry  the  staining  with  the  blue 
just  far  enough,  we  have  a  beautiful  combination 
of  blue  and  red  staining  in  different  objects  and 
different  portions  of  objects.  This  serves  to  show 
up  their  morphology  and  different  parts  to  great 
advantage,  especially  the  endamebae.  There  is 
considerable  difference  in  the  length  of  time 
necessary  to  stain  different  specimens  with  the 
methylene-blue  to  get  the  most  perfect  results, 
but  from  one-fourth  to  one-half  minute  is  suffi- 
cient in  most  cases.  The  film  appears  purple  to 
the  eye  when  properly  stained. 

Examination  of  Stained  Specimens  for  End- 
amebae.— After  the  specimen  has  been  prepared 
and  stained  it  is  ready  for  microscopic  examina- 
tion. Place  a  drop  of  immersion  oil  on  the  film 
and  examine  with  the  oil-immersion  lens.  Select 
a  part  of  the  film  for  examination  that  is  fairly 
thin.  Generally  speaking,  it  is  better  to  search 
for  the  endamebae  in  parts  of  the  film  where  it  is 
only  about  one  cell  thick.  They  can  be  seen  and 
recognized  better  in  such  surroundings  than  where 
the  film  is  much  thicker.  If  the  film  is  made  of 
material  from  exactly  the  proper  part  of  the  lesion, 


Selected  Endamoeba  buccalis  and  other  material  from  pyorrhea  lesions  illustrating 
different  sizes  and  features  found  in  stained  specimens.  These  are  all  camera 
lucida  drawings  from  specimens  stained  with  the  carbolfuchsin  and  methylene- 
blue  stain. 


DIAGNOSIS  105 

often  one  or  more  endamebae  may  be  found  in 
every  field.  On  the  other  hand,  if  the  preparation 
is  made  of  the  pus,  as  it  is  likely  to  be,  and  not 
material  scraped  from  the  bottom  of  the  lesion, 
it  may  be  necessary  to  search  many  fields  during 
several  minutes  before  finding  an  endameba. 

Those  familiar  with  microscopic  examination  of 
material  of  this  kind,  especially  if  familiar  with 
the  appearance  of  stained  specimens  of  other 
endamebae,  will  usually  have  no  difficulty  in 
recognizing  the  Endamoeba  buccalis  and  in  differ- 
entiating them  from  the  other  much  more  numer- 
ous cells,  bacteria,  debris,  etc.,  present.  (See 
Plate  I.) 

The  bacteria  present  are  usually  of  many  differ- 
ent kinds.  Different  species  stain  by  this  method 
blue,  purple,  or  pink.  The  spirochetes,  w^hich  are 
often  present  in  very  large  numbers,  usually  stain 
purple.  Red  blood-cells  stain  pink.  The  pus- 
cells  present  are  chiefly  polymorphonuclear  leuko- 
cytes. In  well-stained  specimens  the  cytoplasm 
stains  pink  and  the  nucleus  stains  purple.  The 
contrast  between  nucleus  and  cytoplasm  is  good. 
Some  epithelial  cells  may  be  present.  Their  cyto- 
plasm stains  pink  and  their  nuclei  purple.  The 
nucleus  is  round  or  oval,  and  is  comparatively 
small,  while  there  is  a  large  amount  of  cytoplasm. 
There  may  also  be  endothelial  or  other  cells  ob- 


io6  ALVEOLODENTAL  PYORRHEA 

tained  from  the  granulating  surface  of  the  gum 
side  of  the  lesion.  They  are  usually  quite  large, 
being  as  large  as,  or  larger  than,  epithelial  cells. 
The  nucleus  is  larger  and  the  cytoplasm  stains  a 
pale  purple. 

Appearance  of  the  Endamebae. — Among  this 
mixture  of  various  kinds  of  cells,  bacteria,  etc., 
endamebae  stand  out  in  striking  contrast  in  most 
instances. 

Endamoebae  buccalis  vary  in  size  from  about 
32  microns  down  to  about  6  microns  in  diameter. 
Some  are  round  or  oval,  others  are  more  or  less 
irregular  in  shape,  depending  largely  upon  the 
rapidity  of  drying  when  the  material  was  spread 
on  the  slide.  Two  parts  of  the  parasite  are  clearly 
shown  by  this  stain — the  endosarc,  or  inner  part, 
and  the  ectosarc,  or  outer  portion.  The  ectosarc, 
which  stains  pink  or  light  purple,  constitutes  a 
covering  of  the  endosarc,  varying  in  thickness  at 
different  places  and  in  different  individuals.  In 
some  places  it  consists  of  an  almost  indistinguish- 
able band,  while  in  other  places  it  may  be  as  thick 
as  one-tenth  to  one-fifth  the  diameter  of  the  para- 
site. In  places  it  may  project  a  considerable  dis- 
tance without  a  corresponding  projection  of  the 
endosarc. 

The  endosarc  stains  blue  or  slightly  purple  and 
there  is  apparently  variation  in  its  density.     The 


Fig.  34. — Photomicrographs  of  selected  Endamoeba  buccalis  representing 
different  sizes,  shapes,  etc.,  in  stained  specimens.  The  large  picture  in  the 
center  is  probably  two  or  three  endamebae.  The  large  parasite  to  the  left 
and  above  contains  1 1  of  the  dark-staining  inclusion  bodies,  about  the  largest 
number  ever  found  in  a  single  parasite. 

107 


io8  ALVEOLODENTAL  PYORRHEA 

shape  is  round  or  oval  or  irregular,  but  is  never 
as  irregular  as  the  ectosarc  arourld  it.  The  endo- 
sarc  contains  a  variable  number  of  very  dark, 
almost  black  stained  bodies.  Some  of  the  smallest 
parasites  may  not  contain  any  of  the  bodies,  while 
the  largest  may  contain  as  many  as  ten.  These 
inclusion  bodies  vary  in  size  from  about  one  to 
three  microns  in  diameter.  Most  of  them  are 
round  or  oval.  Quite  a  few  are  polymorphous, 
resembling  the  nuclei  of  polymorphonuclear  leuko- 
cytes more  or  less  shrunken.  Some  of  these  have 
more  or  less  pinkish  staining  protoplasm  around 
them,  which  still  further  indicates  that  they  are 
leukocytes  or  other  cells.  In  fact,  it  seems  very 
certain  that  these  bodies  are  the  remains  of  cells, 
perhaps  of  different  kinds,  the  cytoplasm  of  which 
is  consumed  or  digested  by  the  parasite.  It  is 
probable  that  the  food  of  the  parasite  consists 
largely  of  these  cells  obtained  from  the  diseased 
tissue.  We  have  often  recognized  them  scattered 
about  free  in  the  preparations.  These  bodies 
attract  attention  to  the  parasites  under  the  micro- 
scope perhaps  as  much  as  any  other  thing.  Usu- 
ally they  appear  even  more  prominently  because 
of  a  clear  ring  (due  to  retraction?)  around  them. 
The  endosarc  also  contains  red  blood-cells  or 
remnants  of  red  blood-cells  in  various  stages  of 
destruction.     These    stain    pink.     They    may   be 


o     % 


5     ^» 


y4 


'^ 


Fig-  35- — Photomicrographs  of  pus  from  different  sources  showing  the 
dark  staining  bodies  apparently  similar  to  those  seen  in  Endamceba  buccalis. 
A,  From  pyorrhea;  B,  chancroidal  gland;  C,  granulating  eczema  surface; 
D,  staphylococcal  infection  of  abraded  surface;  E,  acne  vulgaris.  Note  the 
phagocytosis  of  one  of  these  bodies  by  a  pus-cell  at  the  right. 

109 


no  ALVEOLODENTAL  PYORRHEA 

absent  from  the  smallest  and  some  other  end- 
amebae. 

Bacteria  of  various  sorts  may  be  seen  apparently 
in  both  the  endosarc  and  the  ectosarc  of  some  of 
the  parasites.  Sometimes  they  are  arranged  in 
groups  or  masses.  They  do  not  appear  to  be 
present  in  a  large  portion  of  the  endamebae  in  most 
preparations. 

A  collection  of  chromatin  can  frequently  be 
seen  in  specimens  stained  with  this  stain,  but  it  is 
better  shown  in  specimens  stained  with  the  modi- 
fications of  the  Romanowsky  stain  (Wright's, 
Giemsa's,  etc.).  It  is  round  or  oval,  not  more 
than  one  micron  in  diameter,  and  may  be  situated 
in  most  any  part  of  the  endosarc. 

Examination  of  Unstained  Specimens. — End- 
amebae can  be  diagnosed  with  satisfaction  in 
unstained  specimens  provided  the  examination  is 
properly  made.  The  advantage  of  this  examina- 
tion over  stained  specimens  lies  chiefly  in  the  fact 
that  the  endamebae  are  seen  alive  and  showing 
their  characteristic  ameboid  movement.  On  the 
other  hand,  perhaps  a  little  more  expert  knowl- 
edge of  the  use  of  the  microscope  and  of  the  appear- 
ance of  other  objects  in  such  preparations  is 
required  than  is  required  in  examination  of  stained 
specimens. 

Material  is  obtained  from  the  bottom  of  the 


DIAGNOSIS 


III 


pyorrhea  lesion  or  pocket  in  the  same  way  that 
it  is  obtained  for  stained  specimens.  It  is  diluted 
five  or  ten  times  by  mixing  it  on  a  slide  with  an 
appropriate  quantity  of  patient's  saliva  and  at 
once  covered  with  a  cover-glass.  A  good  plan  is 
first  to  place  about  one-fourth  drop  of  the  saliva 
on  the  slide  at  about  the  middle  of  the  slide. 
Then  obtain  the  material  to  be  examined.  It 
usually  is  a  little  slow  to  come  off  of  the  instru- 
ment and  to  mix  with  the  salt  solution.  A  small, 
common,  hard-wood  toothpick  is  a  very  convenient 
instrument  with  which  the  material  may  be  re- 
moved from  the  point  of  the  dental  scaler  or  other 
instrument  used  to  obtain  it  and  to  facilitate  mix- 
ing with  the  saliva.  Water  may  be  used  instead 
of  the  saliva,  but  the  endamebae  do  not  live  as  long 
in  it. 

The  examination  should  be  made  with  the  high 
dry  or  4  mm.  objective.  Owing  to  the  fact  that 
the  objects  to  be  studied  are  hyaline,  or  have  no 
color  now,  it  is  necessary  to  reduce  the  light  con- 
siderably. This  may  be  done  by  closing  the  iris 
diaphragm  under  the  Abbe  condenser  or  by  lower- 
ing the  condenser  to  some  extent. 

Bacteria  are  usually  very  numerous  and  of 
various  kinds  in  such  preparations.  Some  are 
motile,  others  are  non-motile.  Spirochetes  are 
also  usually  very  numerous,   and   their  activity 


112  ALVEOLODENTAL  PYORRHEA 

attracts  attention.  It  is  quite  possible  that  they 
are  of  considerably  more  importance  as  secondary 
factors  in  producing  pyorrhea  than  the  bacteria 
are. 

There  are  more  or  less  red  blood-cells  in  most 
preparations.  Pus-cells,  chiefly  polymorphonu- 
clear neutrophilic  leukocytes,  are  the  most  nu- 
merous cells  present.  A  few  may  still  be  living, 
but  they  seldom  show  any  considerable  ameboid 
movement.  Their  smaller  size,  small  character- 
istic nuclei,  and  their  granular  cytoplasm  serve 
to  difi^erentiate  them  from  endamebae. 

Epithelial  cells,  which  may  also  be  present,  show 
a  small  round  or  oval,  clear-cut  nucleus,  and 
relatively  large  amount  of  clear  cytoplasm.  They 
are  non-motile. 

Appearance  of  Living  Endamebse. — Endamebae 
first  attract  attention  by  being  larger  than  the 
much  more  numerous  pus-cells  present.  It  is 
true  that  the  smallest  endamebae  are  smaller 
than  pus-cells,  but  whenever  they  are  present 
there  are  also  many  more  of  the  large  parasites, 
many  of  which  are  two  or  three  times  the  diameter 
of  pus-cells.  They  are  more  or  less  irregular  in 
outline  (see  Fig.  36),  and  with  proper  adjustment 
of  the  light  and  close  focusing  the  parasite  is  seen 
to  consist  of  two  separate  portions.  The  ectosarc 
is  clear  greenish  and  quite  homogeneous  in  appear- 


^J^^.. 


Fig.  36. — Large  number  of  selected  living  Endamoebae  buccalis  showing  different 
sizes,  shapes,  etc.,  that  may  be  seen. 
8  113 


Fig-  37. — Drawing  of  an  active  Endamoeba  buccalis,  illustrating  changes  in 
shape  and  position  at  intervals  of  about  one  minute. 


DIAGNOSIS  115 

ance,  while  the  endosarc  is  darker  and  contains 
many  coarse  granules,  cell  detritus,  and  vacuoles. 

If  one  watches  the  parasite  for  a  moment  the 
characteristic  ameboid  movements  may  be  seen. 
A  pseudopod  of  ectosarc  projects  in  one  direction 
and  perhaps  is  retracted  in  a  few  seconds.  Another 
one  may  project  in  another  direction,  and  it  may 
either  be  withdrawn  or  it  may  continue  to  enlarge, 
carrying  with  it  a  part  of  the  endosarc.  Finally 
the  entire  cell  protoplasm  has  flowed  into  the 
pseudopod  and  actually  moved  from  its  original 
position.  In  the  space  of  a  minute  or  two  of  time 
the  most  active  endamebae  may  change  their 
shape  many  times,  and  may  move  the  distance  of 
their  diameter  or  more.  Often  two  or  more 
pseudopodia  may  be  projected  in  diff^erent  direc- 
tions at  the  same  time.  Sometimes  a  pseudopod 
will  be  projected  from  a  pseudopod.  With  a 
little  practice  one  acquires  the  capacity  to  recog- 
nize the  endamebae  when  not  actively  moving,  but 
the  diagnosis  should  be  made  on  these  alone  with 
caution. 

Endamebae  in  such  preparations  live  and  move 
for  several  minutes  or  an  hour  or  two  if  kept  warm. 
If  the  room  is  cold,  they  quickly  cease  motion. 
As  they  die  they  become  round  or  oval  in  shape  and 
clear,    so    that    they    are    difficult    to    recognize. 


ii6  ALVEOLODENTAL  PYORRHEA 

After  a  few  hours  most  of  them  disintegrate  and 
no  other  trace  of  them  can  be  found. 

Dififerentiation  of  Endamoebae  buccalis  from 
Other  Endamebae. — We  do  not  know  of  any 
method  by  which  this  endameba  can  be  differ- 
entiated from  the  many  species  of  amebae  that 
exist  that  would  not  involve  a  knowledge  of 
protozoology  greater  than  this  book  is  intended  to 
convey,  and  far  greater  than  the  authors  possess. 
It  will  require  much  more  study  of  the  protozoa 
of  the  mouth  before  we  will  be  able  to  say  but 
that  what  we  are  now  calling  Endamoeba  buccalis 
may  represent  several  different  species,  which  our 
present  knowledge  does  not  lead  us  to  differentiate. 
It  may  be  possible  that  harmless  species  may  be 
found  in  the  mouth  associated  with  the  patho- 
genic species.  In  one  instance  of  bad  pyorrhea 
in  which  endamebae  having  all  the  appearance  of 
Endamceba  buccalis  were  present  deep  in  the 
lesions,  we  found  large  numbers  of  what  we  took 
to  be  Amceba  coli  on  the  surface  of  the  gums,  well 
up  under  the  lips  and  cheeks.  They  seemed  in 
this  instance  to  be  living  and  reproducing  in  the 
mouth  without  doing  any  harm. 

Apparatus  and  Material  Required  for  Micro- 
scopic Examination. — For  the  benefit  of  those  who 
may  intend  to  prepare  to  make  microscopic  exam- 
inations for  Endamoeba  buccalis,  we  give  here  a 


DIAGNOSIS 


117 


complete  list  of  just  what  we  would  get  for  the 

purpose  under  the  circumstances: 

I.  Microscope,  Bausch  and  Lomb.  B.  B.  8. 
Ocular  X,  Objectives  16  mm.,  4  mm.  (N.  A. 
O.  65),  and  tV  oil-immersion  lens.  This  is  a 
standard  microscope  for  general  clinical  labor- 


Fig.  38. — ^The  apparatus  and  material  required  in  making  microscopic  exami- 
nation for  endameba.     See  list,  pages  117  and  118. 

atory  work.     (Should  have  case  made  to  hold 
microscope  with  mechanical  stage  attached.) 

2.  Mechanical  stage.  Though  this  is  not  es- 
sential, it  is  very  valuable  to  all  except  those 
who  have  had  a  great  deal  of  practice. 

3.  One  box  regular  size,  medium  thickness  micro- 
scope slides. 


ii8  ALVEOLODENTAL  PYORRHEA 

4.  One  box  cover-glasses  J^  inch  square,  No.  2. 

5.  One  or  more  pairs -of  Younger's  dental  scalers 
Nos.  22  and  23. 

6.  A  few  hard-wood  toothpicks. 

7.  One  alcohol  lamp,  or  Bunsen  burner  if  gas 
is  available  and  preferred. 

8.  Two  T.  K.  drop  bottles,  flat  top,  30  c.c.  each. 
The  best  have  the  dropper  come  out  from  the 
side  of  the  top  and  not  from  the  neck  of  the 
stopper  below  the  flat  top. 

9.  Two  fluidounces  carbolfuchsin  (Czaplewsky's 
formula). 

10.  Two  fluidounces  Loflfler's  methylene-blue 
solution. 

Description  of  the  apparatus  and  material 
required  is  given  in  such  detail  for  the  benefit  of 
those  who  are  not  familiar  with  clinical  laboratory 
work,  and  it  should  be  clearly  understood  that 
other  equipment  will  serve  the  same  purpose. 

SUMMARY 

The  history  of  bleeding  gums,  gum-boils,  and 
loose  teeth  and  teeth  changing  position  all  indicate 
pyorrhea. 

On  account  of  the  great  prevalence  of  the  disease 
in  all  adults,  it  should  be  suspected  in  all  grown 
people.  To  suspect  its  presence  is  the  first  thing 
necessary  in  diagnosis. 


DIAGNOSIS  119 

The  endamebae  are  most  numerous  in  the  bottom 
of  lesions,  and  proper  material  for  examination 
can  best  be  obtained  with  a  Younger  scaler  No. 
22  or  No.  23. 

The  endamebae  are  more  easily  demonstrated 
in  stained  specimens  than  in  unstained  specimens. 
The  technic  for  preparing  and  staining  prepara- 
tions is  given  on  pp.  102,  103,  104.  A  list  of  the 
apparatus  and  material  required  for  microscopic 
examination  for  endamebae  is  given  on  pp.  117 
and  118. 

Endamoebae  buccalis  are  from  32  to  6  microns 
in  diameter.  Most  of  them  contain  very  dark- 
staining  inclusion  bodies,  which  are  in  striking 
contrast  to  the  color  of  the  endamebae  and  to  all 
other  material  on  the  slide.  These  serve  to  attract 
attention  to  the  endamebae  and  assist  very  much 
in  finding  them.  We  could  not  give  a  description 
that  would  tell  as  much  about  the  appearance  of 
the  parasites  as  the  several  drawings,  photomicro- 
graphs, and  colored  plate  in  this  book,  to  which 
the  reader  is  referred. 


CHAPTER  VIII 
TREATMENT 

General  Discussion. — The  treatment  of  alveolo- 
dental  pyorrhea  has  for  its  object,  first,  the  destruc- 
tion of  the  Endamoeba  buccalis,  the  specific  cause 
of  the  disease;  and,  second,  the  healing  of  existing 
lesions.  Since  the  damage  done  by  the  disease 
consists  largely  of  destruction  of  structures  and 
tissues,  it  would  seem  that  little  repair  of  the 
damage  done  could  be  expected.  Nature  can  no 
more  grow  new  alveolar  bone  after  it  has  been 
removed  nor  grow  gum  back  onto  the  part  of  a 
tooth  from  which  it  has  retracted  than  she  could 
grow  a  new  tooth  in  place  of  one  that  has  been 
lost  or  a  new  limb  in  place  of  one  that  had  been 
amputated.  For  the  purpose  of  obtaining  the 
first  object  mentioned,  we  are  fortunate  to  have  a 
drug — ipecac — which  is  highly  toxic  to  endamebie 
and  not  harmful  in  proper  doses  to  man. 

It  is  needless  to  explain   that  healing  of  the 

lesions   cannot   reasonably   be   expected    to   take 

place  until  the  cause  has  been  removed.     Though 

we  can  destroy  the  endamebae  with  the  specific, 

ipecac  treatment,  we  have  to  depend  largely  upon 

1 20 


TREATMENT  121 

nature's  processes  for  the  healing  of  the  diseased 
or  damaged  tissue  after  the  cause  has  been  removed. 
Certain  things  can  be  done  to  facihtate  healing, 
however,  and  they  will  be  considered  after  the 
specific  treatment  has  first  been  explained. 

Description  of  Ipecac. — Ipecac  is  the  root  of 
Cephaelis  ipecacuanha  (Richard),  belonging  to  the 
RubiacecB.  The  plant  is  a  small  shrub,  indigenous 
to  Brazil,  and  cultivated  in  certain  other  parts  of 
the  world,  especially  in  India.  It  contains  three 
alkaloids:  emetin  (C15H22NO2),  cephalin  (C14H22- 
NO2),  and  psycotin,  and  certain  gums  or  resins. 
The  action  of  the  drug  seems  to  be  due  entirely 
to  the  alkaloids,  chiefly  emetin  and  cephalin. 

If  ipecac  is  applied  to  the  skin  in  sufficient  con- 
centration and  for  a  sufficient  length  of  time,  it 
finally  causes  ulceration.  Applied  to  the  mucous 
membrane  in  sufficient  concentration,  it  causes 
inflammation  and  ulceration.  When  taken  into 
the  stomach,  nausea  and  vomiting  are  produced, 
apparently  as  the  result  of  local  irritation  to  the 
gastric  mucosa  and  not  of  central  irritation.  Two 
to  five  grains  of  powdered  ipecac  are  sufficient  to 
cause  vomiting  in  most  individuals.  The  effect 
of  a  much  larger  amount  taken  into  the  stomach 
does  not  cause  greatly  increased  symptoms,  be- 
cause the  excess  is  vomited. 

Emetin  has  about  double  the  nauseating  effect 


122  ALVEOLODENTAL  PYORRHEA 

of  cephalin.  Psycotin  is  present  in  small  quantity, 
and  is  not  irritating  to  the  skin  nor  the  mucous 
membrane,  and  is  only  slightly  nauseating,  even 
in  large  doses. 

Both  emetin  and  cephalin  lower  arterial  tension 
when  given  in  sufficiently  large  doses,  emetin 
being  the  more  powerful  of  the  two.  Neither  of 
them  produces  nausea  when  given  hypodermatically 
to  man,  but  in  animals,  as  shown  by  d'Ornellas, 
emesis  is  produced.  Sufficiently  large  doses  given 
hypodermatically  or  intravenously  produce  death 
in  animals,  and  no  doubt  would  do  so  in  man. 
Ten  milligrams  given  intravenously  kills  2000-gram 
rabbits  within  a  few  minutes.  Weakness  and 
collapse  follow  in  two  or  three  minutes.  This  cor- 
responds to  about  0.38  gm.  (6  grains)  for  a  normal 
adult  man. 

Emetin  is  a  non-crystalline,  monacid  base,  but 
forms  crystalline  salts.  The  hydrochlorid  is  the 
one  used  therapeutically.  Cephalin  is  a  crystal- 
line, monacid  base,  and  forms  crystalline  salts. 
Both  are  colorless,  but  are  decomposed  by  light. 
Their  salts  are  stable.  Emetin  was  found  by 
Rogers  to  be  much  the  more  powerful  amebicide, 
and  it  is  therefore  employed  in  preference  to 
cephalin.  Ipecac  is  amebicidal  according  to  the 
amount  of  emetin  it  contains.  Different  samples 
vary  much  in  their  emetin  content.     The  U.  S. 


TREATMENT  123 

P.  standard  requires  that  powdered  ipecac  should 
contain  1.5  per  cent,  total  ether-soluble  alkaloids. 

Manner  in  which  Emetin  Affects  Endamoeba 
buccalis  in  Alveolodental  Pyorrhea. — Emetin  is 
thought  to  be  a  powerful  poison  to  endamebae,  just 
as  quinin  is  a  poison  to  the  malarial  plasmodia. 
Quinin  is  also  toxic  to  man,  and  a  sufficiently  large 
dose  of  quinin  would  kill  a  man  as  certainly  as  a 
sufficiently  large  dose  of  strychnin  would.  Quinin 
is  so  much  more  toxic  to  the  malarial  plasmodia 
than  it  is  to  man,  however,  that  practically  harm- 
less doses  produce  sufficient  concentration  of  the 
drug  in  the  blood  to  kill  the  plasmodia  present. 
The  virtue  of  most  of  our  other  specific  drugs  used 
against  parasitic  diseases  depends  upon  their  capa- 
city to  destroy  the  parasite  with  the  minimum 
amount  of  harm  to  the  patient. 

Emetin  given  hypodermatically  in  doses  so 
small  as  to  produce  no  demonstrable  constitutional 
effect  in  man  furnishes  sufficient  concentration  in 
the  blood  to  eradicate  Endamoebae  buccalis  with 
which  it  comes  in  contact.  This  is  thought  to  be 
because  of  the  specific  toxic  action  of  the  drug  on 
the  endamebae.  It  is  not  equally  toxic  for  other 
protozoa  on  which  we  have  tried  it — malarial  plas- 
modia, trypanosomes,  and  trichomonas. 

Rogers  found  that  emetin  hydrochlorid  was 
amebicidal  in  dilutions  of  i :  100,000  or  less.     Less 


124  ALVEOLODENTAL  PYORRHEA 

than  one-half  grain  given  hypodermatically  to  a 
normal  sized  man  should  theoretically  produce 
more  than  this  concentration  of  the  drug  in  the 
patients*  blood,  and  thus  change  it  to  an  amebicidal 
fluid. 

Emetin  is  slowly  eliminated,  requiring  more 
than  forty-eight  hours  for  the  elimination  of  a 
single  dose.  The  maximum  concentration,  how- 
ever, is  reached  in  about  fifteen  hours.  There- 
fore it  should  not  be  necessary  to  repeat  the  dose 
frequently  to  maintain  a  considerable  concentra- 
tion in  the  blood.  In  this  respect  emetin  is  quite 
different  from  many  other  alkaloids  which  are 
quickly  absorbed  from  the  tissues,  quickly  reach 
the  blood-stream,  and  produce  their  effect,  and 
are  quickly  eliminated. 

Dosage. — Emetin  hydrochlorid  has  been  em- 
ployed for  the  treatment  of  amebic  dysentery  in 
doses  of  from  one-third  to  two  grains.  In  the 
case  of  amebic  dysentery,  the  dose  had  to  be 
determined  more  or  less  empirically.  The  lesions 
containing  endamebae  are  not  accessible  for  fre- 
quent examination  to  determine  just  when  they 
disappear  nor  what  the  effect  of  different  doses  is. 
With  Endamcebae  buccalis  in  pyorrhea  lesions 
which  are  accessible  for  examination  as  frequently 
as  desired,  it  is  possible  to  observe  the  effect  of 
different  sized  doses,  given  with  different  intervals 


TREATMENT  125 

between  doses,  and  the  length  of  time  necessary  to 
eradicate  demonstrable  endamebae.  We  have  done 
considerable  experimentation  with  the  object  of 
shedding  light  upon  these  questions,  controlling 
all  experiments  by  microscopic  examination  for 
the  endamebae.  The  doses  of  emetin  experimented 
with  have  been  from  one-half  to  three  grains.  We 
have  not  been  able  to  determine  that  any  larger 
doses  than  one-half  grain  destroy  the  endamebae 
any  more  quickly  than  this  amount  does.  The 
local  reaction  is  greater  the  larger  the  dose,  and 
the  cost  is  also  proportionately  increased;  there- 
fore it  is  desirable  to  employ  the  minimum  dose 
that  is  certainly  efficient.  At  this  present  writing 
we  think  one-half  grain  of  emetin  hydrochlorid 
given  hypodermatically  is  the  proper  dose  for 
average  sized  adults.  The  dose  may  be  reduced 
for  children  in  proportion  to  age. 

Interval  Between  Doses. — We  have  also  experi- 
mented considerably  to  determine  what  interval 
between  doses  leads  to  the  best  results.  One 
dose  during  a  day  is  about  all  that  would  be  prac- 
tical in  most  instances.  We  have  no  doubt  but 
that  slightly  better  results  might  sometimes  be 
obtained  by  more  frequent  administration  than 
once  a  day,  but  we  do  not  think  the  probable  ad- 
vantage worth  the  inconvenience.  On  the  other 
hand,  we  are  convinced  that  emetin  given  one 


126  ALVEOLODENTAL  PYORRHEA 

dose  every  day  without  intermission  will  destroy 
endamebae  more  certainly  and  quickly  than  when 
an  interval  of  more  than  one  day  is  allowed  to 
intervene  between  doses. 

Technic  of  Giving  Emetin  Hjrpodermatically. — 
Emetin  hydrochlorid  is  the  salt  used  for  this  pur- 
pose. The  most  convenient  form  for  ordinary 
use  is  the  sealed  ampules  containing  one-half 
grain  in  solution  ready  for  use.  It  is  supplied  in 
this  form  by  several  pharmaceutic  houses.  An 
ordinary  hypodermic  syringe  (all  glass  syringes 
are  the  best)  is  sterilized  by  boiling.  The  neck 
of  the  ampule  is  broken,  and  the  contents  are 
drawn  into  the  syringe.  The  injection  is  usually 
made  in  the  arm,  about  the  insertion  of  the  deltoid 
muscle.  A  good  way  to  sterilize  the  skin  where 
the  needle  is  to  be  inserted  is  to  touch  the  skin 
with  a  little  cotton  applicator  moistened  (not  wet) 
with  pure  lysol.  A  place  one-fourth  inch  in  diame- 
ter is  sufficiently  large.  Stick  the  needle  through 
this  and  pretty  deeply.  Make  sure  of  going 
through  all  the  skin.  Less  local  reaction  is  pro- 
duced the  deeper  the  drug  is  placed  intramuscu- 
larly. Inject  the  emetin,  withdraw  the  needle,  and 
wipe  off  the  lysol. 

Local  Effect  of  Emetin. — ^There  is  always  more 
or  less  local  reaction  following  an  injection  of 
emetin.     It  varies  very  much  with  different  indi- 


TREATMENT  127 

viduals,  but  is  generally  worse  in  women  than  in 
men.  There'are  redness  and  soreness  in  an  area  of 
from  about  three-fourths  inch  to  two  inches  in 
diameter.  It  reaches  its  maximum  in  about  two 
days  and  subsides  in  about  three  days.  Sometimes 
there  is  considerable  itching  about  the  fifth  day, 
accompanied  by  formation  of  small  vesicles  and 
shedding  of  epithelium.  We  do  not  know  of  an 
abscess  occurring  in  any  case,  but  we  think  such 
a  thing  may  sometimes  occur. 

Urticaria  Produced  by  Emetin. — ^About  i  per 
cent,  of  the  cases  treated  with  emetin  hypo- 
dermatically  have  developed  general  urticaria. 
It  was  mild  in  all  except  one  case,  in  which  it  was 
quite  severe.  The  urticaria  resembled  that  often 
produced  by  quinin  or  other  drugs,  and  passed 
off  in  from  one  to  three  days.  This  is  an  objection 
to  the  use  of  emetin,  but  the  same  objection  could 
be  raised  to  several  of  our  most  valuable  drugs. 
So  far  as  we  know  and  believe  there  is  no  way  to 
prevent  this,  nor  to  know  in  advance  those  who 
possess  this  idiosyncrasy  to  emetin.  We  have  not 
known  of  its  occurrence  when  the  emetin  was  taken 
internally,  but  should  expect  it. 

Length  of  Time  Necessary  for  Endamebae  to 
Disappear. — The  length  of  treatment  required 
before  the  endamebae  disappear  from  the  lesions 
may  depend  upon  several  factors  that  we  know  of, 


128  ALVEOLODENTAL  PYORRHEA 

and  probably  others  that  we  do  not  now  recognize. 
There  is  considerable  difference  in  the  absorption, 
distribution,  and  elimination  of  drugs  by  different 
individuals,  all  of  which  may  influence  to  some 
extent  at  least  the  effect  of  the  drug.  The  most 
important  source  of  variation,  however,  is  the 
difference  in  the  lesions  in  different  individuals  as 
well  as  in  the  several  lesions  in  the  same  individual. 
Emetin  in  the  blood  eradicates  endamebae  which 
are  in  tissues  bathed  by  the  blood,  but  many  of  the 
endamebae  in  a  pyorrhea  lesion  are  in  dying  and 
dead  tissue  not  well  supplied  with  blood.  It  is 
true  there  is  some  exudation  of  body  fluids  through 
this  material,  but  there  is  no  such  rapid  change  of 
fluids  as  in  the  living  tissue.  Large  pyorrhea 
pockets  contain  a  considerable  amount  of  pus, 
food  particles,  bacteria,  etc.,  in  which  there  are 
also  many  endamebae.  These  substances  are  not 
likely  to  get  much  emetin  from  the  blood.  End- 
amebae often  disappear  within  twenty-four  hours 
after  a  single  dose  of  emetin  from  an  early  lesion 
in  which  all  the  endamebae  are  either  in  living 
tissue  or  directly  in  contact  with  tissues  well  sup- 
plied with  blood.  Emetin  gets  to  them  promptly. 
In  other  more  advanced  lesions  it  requires  longer 
— sometimes  several  days — for  the  contents  of  the 
pyorrhea  pocket  to  become  sufficiently  impreg- 
nated with  the  emetin  to  destroy  all  the  endamebae. 


TREATMENT  129 

This  perhaps  is  especially  true  whenever  it  includes 
spongy  bone  containing  pus  and  endamebae. 

In  our  experience  of  more  than  300  cases  the 
endamebae  disappear  in  from  three  to  six  days  from 
the  time  daily  hypodermatic  treatment  is  begun  in 
all  but  a  small  percentage  of  cases.  In  these  they 
disappeared  in  this  time  from  all  except  perhaps 
one  or  more  lesions  of  extreme  type  in  each  case. 

Treatment  with  Emetin  Injected  into  the  Pyor- 
rhea Pockets. — If  the  reader  is  familiar  with  the 
chapter  upon  Morbid  Process,  it  will  be  clearly 
understood  that  it  would  not  be  practical  or  in 
most  instances  possible  to  find  all  pyorrhea  lesions 
and  to  inject  medicine  into  them  so  as  to  reach  all 
the  endamebae.  A  pyorrhea  pocket  is  practically 
a  deep  ulcer  whose  walls  consist  of  bone  or  tooth 
and  granulating  soft  tissue.*  The  shape  is  such 
as  to  make  it  less  practical  to  reach  all  parts  with 
a  local  application  than  it  would  be  to  reach  all 
parts  of  an  open,  superficial  ulcer  of  the  skin,  for 
instance.  There  are  many  antiseptics  which  we 
can  apply  to  such  an  open  ulcer  of  the  skin  in 
sufficient  concentration  to  kill  bacteria,  but  such 
application  fails  to  disinfect  the  ulcer,  though 
applied  constantly.  The  infection  extends  too 
deep,  speaking  in  microscopic  terms,  to  be  reached 

*  Cavernous  sinuses  extend  into  the  soft  alveolar  process,  and  strands  of 
undissolved  connective  tissue  traverse  the  bottom  of  the  lesion. 


I30  ALVEOLODENTAL  PYORRHEA 

by  the  antiseptic  solution  applied  to  the  surface. 
It  is  no  more  likely  that  we  could  disinfect  a 
pyorrhea  pocket  by  injecting  the  endamebicide 
into  it  than  it  is  that  we  could  disinfect  it  of  bac- 
teria by  washing  it  out  with  an  antiseptic  solution, 
a  thing  that  could  not  be  expected.  Washing  out 
pyorrhea  pockets  with  some  harmless,  non-irritat- 
ing fluid,  preferably  physiologic  salt  solution,  how- 
ever, would  undoubtedly  be  of  value  and  would 
facilitate  healing.  Washing  out  the  pockets 
would  remove  food-particles  that  would  other- 
wise decompose,  accumulations  of  bacteria  that 
sometimes  form  considerable  masses,  pus,  and 
debris,  as  well  as  some  endamebae.  If  emetin  is 
added  to  the  salt  solution  in  proper  quantity,  it 
will  do  no  harm  and  no  doubt  it  will  kill  some 
endamebae.  The  endamebae  washed  out  or  killed 
are  chiefly  those  in  the  dead  material  in  the  lesion, 
and  not  those  deeper  which  are  actually  damaging 
the  tissue.  These  are  the  endamebae,  however, 
that  are  least  likely  to  be  destroyed  by  emetin  in 
the  blood. 

Emetin  diluted  100,000  times  will  kill  endamebae, 
and  therefore  it  is  not  necessary  to  employ  a  strong 
solution  for  this  purpose.  Strong  solutions  of 
emetin  are  irritating  and  tend  to  prevent  healing. 
On  the  other  hand,  it  is  desirable  to  use  a  solution 
sufficiently  strong  that  it  will  still  kill  endamebae 


TREATMENT  131 

after  being  diluted  somewhat  by  the  fluid  secretion 
with  which  it  may  be  mixed  in  the  pocket  or  by 
being  absorbed  into  the  dead  material.  We  think 
a  solution  of  i :  10,000  or  i :  15,000 would  be  harmless 
to  the  tissues  and  still  be  strong  enough  under  all 
circumstances.     This  can  be  made  up  extempo- 


Fig-  39.— Berlin  abscess  syringe  suitable  for  washing  out  pyorrhea  pockets 
with  solutions  of  emetin. 

raneously  and  economically  by  dissolving  a  one- 
half  grain  tablet  of  emetin  hydrochlorid  in  a  pint 
(bottle)  of  salt  solution.  The  salt  solution  may 
be  made  sufficiently  accurate  for  practical  pur- 
poses by  dissolving  60  grains  (one  teaspoonful) 
of  sodium  chlorid  in  a  pint  (bottle)  of  water. 


132  ALVEOLODENTAL  PYORRHEA 

Any  suitable  syringe  may  be  used  for  this 
purpose.  The  best  we  have  seen  is  the  BerHn 
abscess  syringe  (Fig.  39),  which  may  be  obtained 
from  dental  supply  houses  and  some  drug  stores. 
We  have  had  two  patients  to  volunteer  the  infor- 
mation that  after  being  treated  by  their  dentist  by 
injecting  iodin  into  the  pyorrhea  pockets  they  had 
supplied  themselves  with  syringes  and  had  made 
the  injections  themselves.  This  suggested  the 
practicability  of  patients'  washing  out  their  own 
pyorrhea  lesions,  or  having  it  done  by  some  one 
at  the  home,  with  the  emetin  solution.  We  recog- 
nize that  this  can  be  practised  only  by  certain 
patients  and  not  with  all  lesions.  Wherever  prac- 
tical, however,  we  think  it  might  be  found  to  be  of 
considerable  value. 

Barrett  injects  a  0.5  per  cent,  solution  of  emetin 
into  the  pyorrhea  pockets  and  also  infiltrates  the 
surrounding  tissue  with  this  solution,  using  a  hypo- 
dermic syringe  with  proper  needles.  Good  results 
have  been  obtained,  including  rapid  healing  of  the 
lesions  and  disappearance  of  endamebae.  For  the 
treatment  of  individual  lesions,  no  doubt  this 
method  would  give  as  good  results  in  the  hands  of 
skilled  operators  familiar  with  the  disease  as  any 
method.  It  is  doubtful,  however,  whether  it  can 
be  extensively  applied  successfully.  It  would  re- 
quire rather  persistent  use  to  disinfect  the  mouth 


TREATMENT  133 

of  endamebae  in  the  average  case  of  pyorrhea. 
Remember  that  in  addition  to  the  advanced 
recognizable  lesion  there  are  usually  many  others 
in  the  earlier  stages  of  the  disease,  and  some  of 
these  at  least  would  be  difficult  to  locate  and 
treat.  The  greatest  good  will  come  to  the  patient 
from  disinfecting  his  mouth  and  curing  the  earlier 
lesions  as  well  as  those  more  advanced,  which  at 
best  leave  a  tooth  very  much  impaired  in  usefulness 
because  of  the  loss  of  supporting  structures. 

Treatment  with  the  Alkaloids  of  Ipecac  Taken 
Internally  by  Mouth. — ^The  treatment  by  hypo- 
dermatic administration,  though  efficient,  is  neces- 
sarily limited  because  of  the  discomfort  produced, 
the  expense  attached,  etc.  Almost  all  grown 
people  have  the  disease  and  are  doomed  to  lose 
their  teeth  after  years  of  sloughing  and  pus  produc- 
tion around  each  one  of  them,  if  they  live  long 
enough.  Only  a  small  fraction  of  all  the  victims 
of  the  disease  could  or  would  avail  themselves  of 
this  treatment.  Recognizing  these  facts,  we  set 
out  to  find  some  more  practical  and  economic 
method  of  treatment  than  by  administration  of 
the  drug  hypodermatically  or  injection  into  the 
gums,  requiring  expert  service  each  time.  This  we 
now  seem  to  have. 

Alcresta  Ipecac. — ^John  Uri  Lloyd  discovered 
that  a  colloidal  form  of  hydra  ted  aluminum  silicate 


134  ALVEOLODENTAL  PYORRHEA 

possesses  the  power  of  adsorbing  alkaloids  from 
an  aqueous,  neutral,  or  acid  solution.  The  alkaloid 
is  then  not  given  up  except  in  the  presence  of  an 
alkaline  fluid,  when  it  is  promptly  set  free.  The 
only  source  of  the  alkaloids  of  ipecac  prepared  in 
this  way,  so  far  as  we  know,  is  supplied  by  Eli 
Lilly  and  Company  under  the  name  of  "Alcresta 
Ipecac,*'  in  the  form  of  tablets  each  containing  the 
alkaloids  of  lo  grains  of  ipecac.  When  taken  into 
the  stomach  in  this  form,  where  the  reaction  is 
acid,  the  emetin  and  cephalin  remain  inactive 
until  the  alkaline  intestinal  juices  are  reached, 
when  they  are  set  free  and  absorbed.  Quantities 
corresponding  to  50  or  even  100  grains  of  ipecac 
do  not  produce  any  nausea.  The  rate  and  the 
completeness  of  absorption  necessarily  vary  some- 
what with  different  individuals.  Emetin  is  irri- 
tating more  or  less  to  all  tissues.  Certain  indi- 
viduals are  more  susceptible  to  its  action  than 
are  others.  The  irritation  to  the  intestinal  mucous 
membrane  is  sometimes  sufficient  to  give  rise  to 
griping  and  a  little  diarrhea.  We  have  not  seen 
these  symptoms  severe  enough  to  necessitate  the 
patient  discontinuing  the  medicine,  but  we  have 
no  doubt  this  will  occasionally  occur.  In  most 
instances  no  bad  effect  is  noticed.  If  sufficient 
diarrhea  should  be  produced,  there  might  be  so 
little  emetin  absorbed  and  thus  reach  the  blood 


TREATMENT  135 

that  it  would  not  destroy  endamebae  in  the  pyor- 
rhea lesions.     Such,  however,  seldom  occurs. 

The  amount  of  ipecac  necessary  to  contain  one- 
half  grain  of  emetin,  our  regular  hypodermatic 
dose,  is  about  45  grains.  It  usually  requires  about 
twice  as  much  of  a  drug  given  by  mouth  to  have 
the  same  effect  as  when  it  is  given  hypodermatic- 
ally.  Therefore  we  should  give  an  amount  of 
the  Alcresta  Ipecac  representing  about  90  grains 
of  ipecac  per  day.  A  convenient  way  is  for  the 
patient  to  take  three  tablets  three  times  a  day  after 
meals — preferably  one  hour  after  meals. 

We  have  now  tried  it  out  sufficiently  to  state 
that  it  causes  the  disappearance  of  endamebae 
about  as  quickly  as  emetin  given  hypodermatically 
in  a  large  percentage  of  cases.  The  Alcresta  ipecac 
tablets  should  be  continued  for  from  four  to  six 
days  or  longer,  the  same  as  the  hypodermics  of 
emetin.  A  convenient  way  to  write  the  prescrip- 
tion for  them  is — 

I^.     Alcresta  ipecac  tablets  (Lilly),  40. 

Label. — Three  tablets  three  times  a  day  an  hour  after  meals. 

Forty  is  about  the  number  required  for  a  course 
for  the  average  case,  and  the  manufacturers  sup- 
ply them  in  original  bottles  containing  40  tablets 
each. 

Alcresta  Emetin. — Since  the  cephalin  and  psy- 
chotin  are  also  contained  in   the  Alcresta  ipecac 


136  ALVEOLODENTAL  PYORRHEA 

tablets,  we  have  recently  had  the  manufacturers 
make  for  us  Alcresta  emetin  instead  of  Alcresta 
ipecac  (combined  alkaloids).  It  was  hoped  that 
the  slight  discomfort  of  griping  and  looseness  of 
the  bowels  might  not  be  produced  by  this  prepara- 
tion. This  matter  is  still  under  investigation. 
Relapse  or  Reinfection. — As  a  result  of  a  proper 
course  of  from  four  to  six  days  or  more  of  emetin 
treatment,  we  are  unable  to  find  endamebae  in  the 
lesions  except  perhaps  in  a  small  percentage  of 
cases,  and  usually  only  in  certain  bad  lesions.  It  is 
not  possible  to  say  that  no  endamebae  remain.  We 
can  only  say  that  they  have  been  reduced  to  such 
small  numbers  that  they  are  not  demonstrable,  or 
else  they  have  entirely  disappeared.  It  may  per- 
haps be  desirable  for  us  to  explain  why  we  advise 
to  discontinue  the  internal  administration  of  eme- 
tin as  soon  as  the  demonstrable  endamebae  disap- 
pear, instead  of  continuing  it  longer.  The  pain  and 
expense  accompanying  the  hypodermatic  treat- 
ment make  it  desirable  not  to  continue  the  treat- 
ment any  longer  than  necessary.  The  intestinal 
disturbance  sometimes  produced  by  the  Alcresta 
ipecac  (alkaloids)  is  one  reason  for  desiring  to  dis- 
continue it  as  soon  as  it  is  no  longer  needed.  The 
Alcresta  emetin  may  not  have  this  objection  to  the 
same  extent,  but  there  is  another  reason  applicable 
to  all  forms.     Many  alkaloids,  whenever  taken  for 


TREATMENT  137 

more  than  a  few  days  at  a  time,  rapidly  lose  their 
effect.  They  are  either  neutralized  or  eliminated 
without  getting  into  the  blood  in  the  same  con- 
centration that  they  did  when  first  taken.  The 
maximum  effect  is  obtained  when  the  alkaloid  is 
taken  for  only  a  few  days,  and  repeated  if  neces- 
sary after  an  interval  of  at  least  a  few  days.  We 
do  not  want  to  set  the  course  of  treatment  arbi- 
trarily at  four  to  six  days.  We  simply  say  it  is 
sufficient  for  most  cases,  but  we  have  no  doubt  but 
that  a  longer  course  will  be  found,  sometimes,  at 
least,  more  successful.  In  fact,  we  feel  that  if  we 
were  deprived  of  the  microscopic  examination 
with  which  to  control  the  progress  of  treatment, 
we  would  be  inclined  to  make  the  course  of  treat- 
ment longer,  perhaps  ten  days  or  two  weeks  in  the 
worst  cases. 

Though  the  specific  emetin  treatment  causes 
the  disappearance  of  demonstrable  endamebae,  the 
lesions  or  pockets  remain  and  will  require  days, 
weeks,  or  months  to  heal,  depending  largely  upon 
the  size,  extent,  and  nature  of  the  individual  lesions 
as  well  as  upon  the  natural  healing  powers  of  the 
individual  patient.  In  many  lesions  there  is  con- 
siderable alveolar  bone  denuded  of  its  periosteum, 
which,  therefore,  must  be  removed  by  the  long, 
slow  process  of  nature,  if  not  aided  by  artificial 
mechanical    means.     It    requires    nature    several 


138  ALVEOLODENTAL  PYORRHEA 

months  to  absorb  and  remove  the  alveolar  bone 
after  a  tooth  has  been  extracted,  and  it  requires 
several  months  also  to  remove  the  alveolar  bone 
above  the  level  of  the  living  peridental  membrane 
in  the  case  of  pyorrhea.  After  the  endamebae 
have  been  destroyed  and  the  blood  no  longer 
contains  emetin,  these  lesions  or  pockets  offer 
the  most  favorable  soil  for  reinfection. 

This  disease  is  almost  universal.  Nearly  every- 
body has  the  infection  and  is  throwing  off  end- 
amebae with  the  secretions  of  the  mouth  at  frequent 
intervals.  With  our  present  habits  of  drinking 
and  eating  after  each  other  and  putting  things  into 
our  mouths  that  have  been  exposed  to  infection  by 
others,  we  must  be  putting  endamebae  into  our 
mouths  almost  daily.  With  several  healing  pyor- 
rhea pockets  in  the  mouth  offering  most  favorable 
places  for  lodgment  of  endamebae,  it  could  hardly 
be  reasonably  expected  that  one  would  go  many 
days  without  getting  reinfected.  Reinfection  es- 
tablished in  one  place  would  be  a  source  of  rein- 
fection of  other  lesions  as  soon  as  the  endamebae 
have  time  to  multiply  sufficiently.  This  would 
seem  to  take  away  the  promise  of  complete  cure 
by  use  of  emetin  unless  it  is  repeated  at  frequent 
intervals.  We  have,  however,  been  able  to  elim- 
inate this  discouraging  feature,  to  some  extent,  at 
least,    by   prophylactic    measures,    especially    the 


TREATMENT  139 

local  use  of  ipecac  or  emetin  by  the  patient.  The 
reader  is  invited  to  turn  to  page  160,  where,  under 
the  heading  "Local  use  of  emetin  as  a  prophylac- 
tic," this  subject  is  fully  discussed.  Emetin  used 
in  this  way  would  tend  to  prevent  reinfection. 
It  could  not,  however,  be  expected  to  furnish 
absolute  protection,  because  endamebae  may  be 
introduced  at  any  time  of  the  day  or  may  be  intro- 
duced deeply,  while  the  emetin  is  used  only  one 
or  two  or  three  times  a  day  and  cannot  reach  deeply 
situated  endamebae.  In  addition  to  the  pro- 
phylactic use  of  emetin  to  prevent  reinfection, 
patients  should  endeavor  to  minimize  the  intro- 
duction of  endamebae  according  to  the  sugges- 
tions made  in  the  chapter  upon  Prophylaxis,  page 
144. 

In  spite  of  our  prophylaxis,  we  may  expect  a 
certain  percentage  of  cases  to  get  reinfected  long 
before  nature  could  heal  all  the  lesions  present. 
In  our  experience,  endamebae  are  demonstrable 
in  some  of  the  lesions  in  at  least  12  or  15  per  cent, 
of  cases  in  from  three  to  six  weeks  after  all  had 
apparently  been  destroyed.  It  is  not  possible 
to  determine  whether  these  are  cases  of  reinfec- 
tion or  cases  in  which  all  endamebae  had  never 
been    destroyed,    and    therefore    more    correctly 


I40  ALVEOLODENTAL  PYORRHEA 

called  cases  of  relapse.*  On  account  of  the  con- 
siderable number  of  reinfections  or  relapses,  as 
the  case  may  be,  that  occur,  we  believe  it  advisable 
that  the  course  of  emetin  should  be  repeated  after 
an  interval  of  from  two  to  four  weeks  in  all  cases, 
unless  thorough  microscopic  examination  is  made 
and  no  endamebae  found  present.  The  courses 
of  emetin  should  be  repeated  again  and  again 
until  all  the  lesions  heal. 

Scaling  and  Scraping  the  Roots  of  Teeth. — 
If  a  tooth  surrounded  by  a  pyorrhea  pocket  is 
extracted  and  examined,  considerable  accumu- 
lation of  deposit  of  various  kinds  is  found  on  the 
part  of  the  root  that  was  between  the  level  of  the 
edge  of  the  gum  and  the  edge  of  the  remaining  peri- 
dental membrane.  This  may  be  either  soft  or 
hard.  There  is  a  deep-set  opinion  held  by  the 
dental  profession  that  it  is  important  to  scale  or 
scrape  this  off  to  facilitate  healing.  This  might 
be  true  if  there  was  any  hope  that  the  destroyed 
peridental  membrane  would  be  regrown  and 
again  cover  the  root  of  the  tooth  where  it  for- 
merly existed.  We  have  not  the  slightest  evi- 
dence, however,  that  such  a  thing  can  occur. 
Apparently,  therefore,  the  only  benefit  that  would 


*  Though  we  have  not  been  able  to  demonstrate  it,  we  think  it  quite  pos- 
sible that  encysted  endamebae  in  the  tissues  escape  the  effect  of  emetin,  and 
after  it  gives  way,  reproduce  and  give  rise  to  another  crop  of  the  parasites. 


TREATMENT  141 

result  would  be  what  results  from  cleanliness  and 
removal  of  foreign  material,  which  may  in  some 
instances  be  a  source  of  irritation.  However,  if 
done  properly,  no  harm  should  result. 

Removal  of  Redundant  Tissue. — In  many  pyor- 
rhea lesions  we  have  alveolar  bone  denuded  of 
periosteum  projecting  upward  by  the  side  of  or 
around  the  tooth.  This  bone  can  never  be  re- 
covered with  periosteum  and  will  certainly  be 
removed  by  nature  by  a  long,  slow  process  of  lique- 
faction. This  requires  months  in  many  cases, 
when  it  could  be  done  at  once  by  surgical  pro- 
cedure. The  results  to  be  expected  from  such 
operation  done  now  are  not  to  be  compared  with 
what  may  have  been  obtained  when  it  was  tried 
before  we  knew  the  specific  cause  of  the  disease 
and  had  a  specific  remedy  against  it.  Cutting 
away  redundant  gum  that  helps  to  make  the 
pocket  ought  also  very  much  to  facilitate  the  heal- 
ing process.  If  left  to  nature,  it  finally  retracts 
to  the  level  of  living  peridental  membrane,  to 
which  the  edge  of  it  is  finally  united.  As  long  as 
the  pocket  is  present  it  collects  food  and  retains 
material  from  deeper  down,  which  decomposes 
and  keeps  up  irritation.  The  real  disease  is  in 
the  very  bottom  of  the  lesion,  and  converting  the 
pocket  into  a  wide-open,  freely  draining  lesion 
very  much  facilitates  healing. 


142  ALVEOLODENTAL  PYORRHEA 

Though  we  have  not  had  sufficient  observation 
to  be  able  to  recommend  the  operation  of  remov- 
ing gum  and  bone  that  nature  finally  removes,  we 
believe  that  it  is  the  proper  thing  to  do.  One 
obstacle  will  be  met  in  most  cases,  and  that  is 
objection  on  the  part  of  the  patient.  It  will  not 
be  easy  to  get  patients  and  others  to  appreciate 
the  real  extent  of  the  disease,  and  the  fact  that 
the  overhanging  bone  and  gum  will  finally  be 
removed  by  nature  anyhow.  We  are  now  able  to 
explain  the  certain  amount  of  success  formerly  ob- 
tained by  difi^erent  "pyorrhea  specialists**  by  cut- 
ting down  the  gum  and  often  cutting  it  away  and 
by  the  application  of  acids  into  the  pyorrhea 
pockets. 

Supporting  Teeth  that  are  Loose  or  Have  not 
SuflBlcient  Support  to  Give  Them  Strength. — It 
frequently  happens  that  a  tooth  or  several  teeth 
are  more  or  less  loose  as  a  result  of  the  great  depth 
to  which  the  peridental  membrane  has  been  de- 
stroyed. Healing  and  repair  are  prolonged  by  the 
strains  to  which  the  little  remaining  supporting 
structures  are  subjected.  Steadying  such  teeth 
so  they  cannot  move  about,  by  binding  them  to 
other  teeth  in  such  a  way  as  the  individual  case 
requires,  may  often  be  done  to  great  advantage. 
In  fact,  some  teeth  may  be  saved  whose  insertion 
into  the  supporting  structures  may  be  so  shallow 


TREATMENT  143 

after  retraction  is  complete  that  they  will  not 
stand  up  in  their  natural  position,  in  which  case 
permanent  attachment  to  other  teeth  may  be 
indicated.  We  shall  not  enter  into  any  discussion 
of  the  many  methods  of  accomplishing  this  object, 
and  which  are  familiar  to  all  dentists. 

Note. — Since  our  early  publications  we  have  seen  a  considerable  num- 
ber of  cases  in  which  endamebas  have  reappeared  after  they  had  been  absent 
for  various  periods  of  time  following  the  use  of  emetin  in  one  way  or  another. 
We  have  also  seen  a  considerable  number  of  cases  in  which  endamebas  have 
not  been  eradicated  even  for  a  short  time  by  emetin.  We  know  of  instances 
in  which  endamebas  disappeared  from  individual  lesions  as  a  result  of  local 
use  of  emetin  after  emetin  given  hypodermatically  had  failed  to  get  rid  of 
them.  This  all  goes  to  show  that  the  methods  of  specific  treatment  now 
followed  fall  far  short  of  the  ideal  and  that  further  experience  should  lead  to 
great  improvement.  No  doubt  it  will  be  found  that  there  is  good  in  both 
local  and  systemic  use  of  emetin  at  the  same  time  in  most  cases. 

We  do  not  want  to  be  understood  as  underestimating  the  value  of  proper 
dental  treatment  of  any  abnormal  condition,  whether  it  be  the  result  of 
alveolodental  pyorrhea  or  other  diseases  or  abnormalities  of  the  teeth  and 
supporting  structures.  We  have  not  taken  up  the  surgical  treatment  of 
pyorrhea  because  the  methods  that  have  been  employed  are  familiar  to  the 
dental  profession  and  are  described  in  the  dental  Hterature,  and  because  no 
new  methods  have  yet  been  worked  out  in  the  light  of  our  recently  acquired 
knowledge  of  the  specific  cause  of  the  disease.  It  remains  for  future  investi- 
gation to  indicate  the  proper  surgical  treatment  to  be  combined  with  the 
specific  emetin  treatment. 


CHAPTER  IX 
PROPHYLAXIS 

The  reader  should  read  at  least  the  chapters 
on  Etiology  and  on  Morbid  Process  before  reading 
this  one,  unless  he  is  already  familiar  with  the 
specific  cause  of  the  disease,  the  manner  in  which 
endamebae  produce  the  disease  process,  and  the 
nature  of  the  process. 

Care  of  the  Teeth  to  Prevent  Development  of 
Favorable  Soil  for  Infection. — As  has  been  pointed 
out,  the  destructive  disease,  alveolodental  pyor- 
rhea, is  caused  by  a  specific  living  microscopic 
animal  parasite,  Endamceba  buccalis  (and  possibly 
other  species),  which  lives  as  a  parasite  in  the 
affected  tissues.  These  endamebae,  however,  are 
harmless  when  applied  to  normal  gums  and  tissues. 
They  cannot  take  hold  and  establish  themselves  on 
normal  mucous  membrane  any  more  than  tetanus 
bacilli  applied  to  the  normal  skin  could  produce 
tetanus.  Not  only  must  tetanus  bacilli  be  intro- 
duced into  the  tissue,  but  that  tissue  must  be  dam- 
aged, crushed,  dying,  or  dead  to  constitute  favor- 
able soil  for  the  organism   to  start  growing  in. 

Many  other  disease-producing  organisms,  some  of 

144 


PROPHYLAXIS  145 

them  of  the  most  virulent  type,  are  not  capable 
of  producing  their  disease  when  applied  to  normal 
unbroken  skin  or  mucous  membrane,  for  instance, 
plague  bacillus,  rabies  virus,  vaccine  virus,  Trepo- 
nema pallida,  Leishmania,  etc. 

Endamceba  buccalis  as  a  parasite  of  man  has 
been  accustomed  to  growing  in  a  certain  kind  of 
tissue  and  environment  for  countless  generations. 
This  has  been  so  for  so  long  a  time  that  it  is  more 
or  less  a  fixed  requirement  of  the  species.  It  is 
not  healthy  tissue  that  they  have  been  accustomed 
to  live  in,  but  it  is  dead,  dying,  and  diseased  tis- 
sue constantly  irritated  by  food-particles  and  bac- 
terial action  and  the  action  of  the  endamebae 
themselves.  Their  food  is  largely  broken-down 
tissue  and  especially  certain  pus-cells.  If  we  could 
in  some  way  remove  all  the  endamebae  from  a 
pyorrhea  lesion  in  which  they  are  living  and  repro- 
ducing in  their  natural  way,  and  not  alter  the 
lesion  or  its  contents,  we  would  have  left  present 
the  most  favorable  soil  for  endamebae.  No  better 
soil  could  be  found  than  that  in  which  the  para- 
site naturally  grows.  Such  soil,  consisting  of 
damaged  peridental  membrane  with  a  little  pus 
formation,  microscopic  in  quantity,  perhaps,  plus 
bacteria  and  food-particles,  can  be  produced  in  a 
number  of  ways. 

Use  of  the  Toothpick  Dangerous. — Picking  the 
10 


146  ALVEOLODENTAL  PYORRHEA 

teeth  often  damages  the  gum.  The  soft  tissue 
may  be  torn  away  from  the  tooth  sufficiently  to 
cause  the  flow  of  a  Httle  blood,  and  if  we  would 
examine  carefully  at  once,  we  might  be  able  to 
recognize  a  little  wound  or  pocket  by  the  side  of 
the  tooth.  It  is  not  necessary,  however,  that  the 
wound  should  be  large  enough  to  be  seen  by  the 
unaided  eye.  A  very  small  wound  would  be  suffi- 
ciently large  to  hold  microscopic  particles  of  food, 
many  bacteria,  and  many  endamebae.  Picking 
the  teeth  should,  therefore,  be  avoided,  and  when- 
ever thought  absolutely  necessary,  it  should  be 
done  with  great  care  not  to  wound  the  gums.  The 
instances  in  which  it  is  necessary  to  use  tooth- 
picks are  extremely  few. 

Dental  Floss  and  Rubbers. — Cleaning  the  teeth, 
as  is  often  practised,  by  passing  dental  floss,  thread, 
or  a  rubber  strip  between  them,  often  damages 
the  tissue  at  the  attachment  of  the  gum  to  the 
tooth.  Considerable  force  is  sometimes  required 
to  pass  the  cord  between  the  teeth  where  the 
crowns  are  normally  in  close  apposition,  and  conse- 
quently when  it  does  slip  through,  it  strikes  the 
interdental  gum  with  considerable  force,  often 
sufficient  to  wound  the  soft  tissue.  Who  ever 
cleaned  all  his  teeth  in  this  way  without  drawing  a 
little  blood.?  Bleeding  always  means  a  break  or 
wound  in  the  tissue.     True,  such  a  wound  may 


PROPHYLAXIS  147 

be  very  small,  but  it  is  of  ample  size  to  furnish 
lodgment  for  many  endamebae.  We  do  not  believe 
the  use  of  such  means  to  clean  the  teeth  is  advis- 
able, except  perhaps  in  extremely  rare  instances, 
when  they  should  be  employed  with  great  care. 
We  are  fully  aware  of  the  fact  that  this  is  contrary 
to  the  general  opinion  and  advice,  but  we  believe 
that  in  the  light  of  present  information  the  latter 
opinion  and  advice  appear  to  be  incorrect. 

Brushing  the  teeth  is  often  a  source  of  damage 


Fig.  40. — An  ordinary  tooth-brush  from  which  the  bristles  shown  in  Fig.  41 

were  taken. 


that  should  be  avoided.  The  ordinary  coarse 
bristle  tooth-brush,  when  vigorously  used,  may 
be  quite  a  source  of  trauma  to  the  gums.  Though 
the  bristles  are  simply  coarse  hairs,  and  appear 
harmless  if  we  look  at  them  with  the  unaided  eye, 
whenever  examined  under  considerable  magnifi- 
cation with  the  microscope  the  end  of  each  one 
resembles  a  coarse  nail,  and  many  of  them  very 
sharp  pointed  at  that.  If  one  presses  such  a 
brush  against  the  closed  teeth  he  feels  a  pricking 
or  sticking  sensation  at  the  edge  of  the  gum.     True» 


148 


ALVEOLODENTAL  PYORRHEA 


it  is  not  very  painful.  The  normal  gum  is  not 
very  sensitive  to  pain.  The  sticking  sensation  is 
due,  however,  to  the  sharp  ends  of  some  of  the 


Fig.  41. — Photomicrograph  of  bristles  taken  from  the  tooth-brush  shown 
in  Fig.  40.  Could  it  be  possible  to  brush  the  teeth  (and  gums)  with  such  an 
instrument  without  damage  to  the  gums? 


bristles  sticking  in  the  gum,  and  especially  at  the 
line  of  attachment  to  the  tooth  by  the  peridental 
membrane.  The  little  wounds  made  by  the 
bristles  are  very  small, — microscopic,   in  fact, — 


PROPHYLAXIS  149 

but  they  are  still  large  enough  to  furnish  a  favor- 
able field  for  the  inoculation  of  several  endamebae 
if  they  chanced  to  be  introduced  at  the  proper 
time.  It  is  true  that  many  such  wounds  heal  very 
quickly.  If  one  brushes  the  teeth  (and  gums) 
vigorously  with  such  a  brush,  there  are  often  so 
very  many  of  such  little  wounds  produced  that 
more  or  less  bleeding  occurs. 

The  finer  and  softer  the  bristles  of  the  tooth- 
brush, the  less  damage  is  done,  but  perhaps  it  is 
almost  impossible  to  avoid  doing  at  least  a  little 
damage,  especially  if  the  brush  is  drawn  across 
the  teeth.  Much  less  damage  would  be  done,  it 
would  seem,  if  the  brush  is  drawn  from  above 
downward  in  brushing  the  upper  teeth  and  from 
below  upward  in  brushing  the  lower  teeth. 

The  frequency  with  which  the  teeth  are  brushed 
is  of  some  importance.  If  a  certain  amount  of 
damage  is  done  each  time,  then  it  would  be  impor- 
tant not  to  brush  the  teeth  more  frequently  than 
is  necessary.  This  leads  us  to  inquire  for  what 
purpose  the  brushing  is  done.  We  think  of  two — 
to  remove  or  prevent  accumulation  of  tartar  con- 
sisting of  mucus,  bacteria,  and  other  substances  on 
the  teeth;  and  to  remove  food-particles  from 
around  and  between  the  teeth. 

Removal  of  Tartar. — For  the  purpose  of  remov- 
ing tartar  it  could  hardly  be  argued  that  brushing 


ISO  ALVEOLODENTAL  PYORRHEA 

more  frequently  than  once  each  day  is  necessary. 
The  heroic  brushing  to  which  many  people  sub- 
ject their  teeth  (and  gums)  several  times  each  day 
is  hardly  warranted  for  this  purpose.  It  is  quite 
probable  that  tartar,  if  soft,  can  be  removed  as 
effectually  by  rubbing  the  teeth  with  a  suitable 
piece  of  gauze  or  cloth  and  without  damaging  the 
gums  as  the  brush  usually  does.  Or  perhaps  some 
genius  will  invent  some  other  instrument  which 
will  serve  this  purpose. 

Brushing  to  remove  food  is  only  partially  suc- 
cessful and  not  necessary.  Food  in  the  form  of 
grease  and  very  small  particles  may  adhere  to  the 
surface  of  teeth,  and  after  a  meal  the  teeth  feel 
just  a  little  less  smooth  on  the  surface  due  thereto. 
A  few  strokes  with  the  brush  remove  this  and 
put  a  cleaner  feeling  in  the  mouth  than  before. 
Most  of  the  roughness  is  washed  away  by  the 
saliva  in  an  hour  or  two  if  let  alone,  or  it  could  be 
removed  with  a  suitable  piece  of  gauze  without 
injuring  the  gums,  as  the  ordinary  brush  does. 
For  the  purpose  of  removing  food-particles  from 
between  the  teeth  the  most  vigorous  brushing  is  a 
failure.  The  brush  does  not  reach  much  of  the 
material  it  is  desired  to  remove.  This  can  be 
accomplished  much  more  effectually  by  thoroughly 
rinsing  the  mouth  by  forcing  water  between  the 
teeth  several  times.     We  therefore  question  the 


PROPHYLAXIS  151 

advisability  of  brushing  the  teeth  with  a  bristle 
brush  for  the  purpose  of  removing  food-particles. 
In  the  event  it  is  employed  it  should  be  done  with 
great  care. 

Polishing  Powders  and  Pastes. — Various  pow- 
ders, either  as  dry  powder  or  incorporated  in 
pastes,  are  used  for  the  purpose  of  polishing  and 
cleaning  the  teeth.  Chalk  and  pumice  are  the 
chief  ones.  Any  of  them  to  be  effectual  must  be 
gritty,  but  it  may  be  that  the  powder  is  so  fine 
that  its  gritty  nature  is  not  appreciated  on  ordin- 
ary examination.  Under  the  microscope,  however, 
such  material  can  be  seen  to  consist  of  irregularly 
shaped,  sharp-cornered,  sharp-edged,  and  sharp- 
pointed  particles.  Power  to  polish  depends  upon 
this.  Such  material,  placed  on  the  ordinary 
tooth-brush  and  used  moderately,  may  not  injure 
the  enamel  of  a  normal  tooth — the  enamel  is  so 
hard.  It  is  quite  different  with  the  soft  edge  of 
the  gum,  which  yields  much  more  readily  to  such 
grinding  or  rubbing.  A  little  damage  is  done, 
some  cells  are  rubbed  away,  and  perhaps  if  we 
could  examine  microscopically  we  would  find  the 
superficial  layer  of  epithelial  cells  removed  and 
blood-cells  passing  out  through  the  damaged  tissue. 
Repair  of  such  damage  is  so  rapid  that  the  harm 
done  ordinarily  is  not  great  unless  the  perform- 
ance is  repeated  too  often.     Some  people,  in  their 


152 


ALVEOLODENTAL  PYORRHEA 


zeal  to  keep  their  teeth  scrupulously  clean,  grind  or 
damage  the  gums  in  this  way  several  times  a  day. 
Before  the  damaged  tissue  has  had  time  to  be 
repaired  by  nature's  processes  it  is  again  subjected 


KyTPirmfr^,. 


^.^ 


■vf^ 


Fig.  42. — Photomicrograph  of  prepared  chalk  from  one  of  the  common 
tooth-powders.  Imagine  brushing  the  teeth  (and  gums)  with  such  a  brush 
as  that  pictured  in  Figs.  40  and  41,  and  with  this  sharp,  gritty  material  on  it. 
Not  only  would  it  damage  the  gum  and  cause  retraction,  but  it  would  wear 
away  grooves  in  the  root  of  the  tooth  after  it  is  exposed.  Most  other  powders 
and  pastes  that  are  effective  "cleansers"  contain  similar  gritty  material. 
This  is  the  chief  cause  of  "erosion." 


to  the  same  trauma.  By  proper,  delicate  technic 
we  can  remove  with  a  suitable  small  instrument 
a  very  small  amount  of  secretion  from  the  edge 


PROPHYLAXIS  153 

of  the  gum  where  it  is  attached  to  the  tooth  of  an 
individual  who  uses  these  substances  vigorously, 
provided  the  teeth  have  not  been  brushed  during 
the  preceding  hour  or  two.  Though  this  material 
is  insignificant  in  quantity,  a  microscopic  examina- 
tion shows  it  to  contain  many  pus-cells.  Pus  is 
not  thrown  off  by  a  normal  or  unbroken  tissue. 
In  addition,  we  can  also  often  recognize  some  of 
these  sharp,  gritty  particles  which  have  been 
rubbed,  as  it  were,  into  the  soft  tissue.  Actually 
the  edge  of  the  gum  is  kept  in  more  or  less  of  an 
ulcerated,  inflamed  condition  from  which  pus  is 
being  thrown  off.  Though  the  extent  of  the 
damage  may  not  be  sufficiently  great  to  attract 
attention,  or,  in  fact,  to  be  recognized  without 
microscopic  examination,  it  exists,  nevertheless. 

This  continued  grinding  and  damaging  of  the 
gums  results  in  wearing  them  back  slowly,  but 
surely,  if  sufficiently  vigorously  practised.  Such 
damaged  gums  offer  favorable  soil  for  Endamcebae 
buccalis.  Tooth-powders  and  pastes  containing 
powders  are  therefore  harmful,  and  may  be  a 
source  of  alveolodental  pyorrhea.  It  may  be 
advisable  to  polish  the  teeth  once  in  a  great  while 
with  such  preparations,  in  which  instance  it 
should  be  done  with  cate. 

Erosion  of  Teeth  Caused  by  Brushing  with 
Powders. — Though    not    directly    bearing    upon 


154  ALVEOLODENTAL  PYORRHEA 

pyorrhea,  it  perhaps  is  permissible  for  us  to  point 
out  in  connection  with  powders  and  pastes  con- 
taining gritty  substances  the  fact  that  a  very 
important  condition  of  the  teeth,  erosion,  is  pro- 
duced chiefly  by  their  use.  Though  the  enamel  of 
the  tooth  is  hard  and  not  ordinarily  damaged  by 
rubbing  with  gritty  substances,  the  neck  and  root 
exposed  from  brushing  or  pyorrhea  are  much 
softer,  and  vigorous  brushing  finally  grinds  away 
trenches  or  depressions  in  the  part  most  exposed. 
Erosion  is  caused  in  this  way. 

We  have  on  several  occasions  advised  persons  to 
quit  the  use  of  pastes,  powders,  and  dentifrices, 
and  in  most  instances  the  question  was  asked, 
"What  must  I  use  to  clean  my  teeth  and  remove 
the  bad  taste.?"  Most  people  who  try  to  take 
care  of  their  teeth  use  some  one  or  more  of  the 
many  patent,  proprietary,  or  other  preparations  as 
a  habit,  and  imagine  that  they  are  very  essential. 
Little  do  they  realize  that  the  bad  taste  they 
relieve  by  their  use  is  the  result  of  damage  done 
by  previous  use  of  the  same  preparation.  The 
amount  of  money  that  is  worse  than  wasted  in  the 
United  States  annually  for  the  many  harmful 
preparations  of  this  kind  would  be  astounding  if 
we  knew  what  it  was. 

Ill-fitting  Dental  Work. — Whenever  consider- 
able pressure  is  made  on  soft  tissue,  like  the  gum. 


PROPHYLAXIS  iSS 

for  a  sufficient  length  of  time,  inflammation  and 
ulceration  result.  A  crown  forced  against  the 
gum,  as  they  usually  are,  soon  produces  such  a 
condition,  especially  if  the  gum  is  torn  away  from 
the  tooth  to  some  extent  at  the  time  it  is  put  on. 
Such  ulcerated  lesion  furnishes  favorable  soil  for 
Endamoebae  buccalis.  Sometimes  the  rough  edge 
of  a  filling  extends  into  the  gum,  causing  inflamma- 
tion and  ulceration.  Other  ill-fitting  dental  work 
may  also  be  a  source  of  damage  to  the  soft  tissues, 
producing  tissue  subject  to  infection  by  endamebae. 
During  our  studies  of  pyorrhea  we  do  not  recall 
having  seen  a  single  cap  crown  that  was  not  irri- 
tating the  gum  more  or  less.  There  has  been 
pus  at  the  edge  of  the  gum  in  contact  with  the 
metal  in  every  instance  we  have  examined.  We 
are  not  informed  whether  crowns  can  be  put  on 
without  doing  this  damage,  but  if  they  cannot, 
they  must  be  recognized  as  a  fruitful  source  of 
harm. 

Salivary  Calculi. — We  are  in  considerable  doubt 
at  this  time  as  to  the  cause  of  salivary  calculi. 
They  either  cause  irritation,  inflammation,  and 
ulceration  of  the  gums,  or  the  disease  of  the  gums 
produces  the  deposit.  We  have  not  been  able 
to  find  a  single  instance  where  there  was  not  micro- 
scopic or  macroscopic  pus  present  at  the  edge  of 
the  gum,  and  in  a  large  percentage  of  cases  end- 


iS6  ALVEOLODENTAL  PYORRHEA 

amebae  have  been  found  also.  The  condition  of 
the  gum  around  a  calculus  is  favorable  for  infec- 
tion with  Endamcebae  buccalis.  Removal  or  pre- 
venting these  calculi  would,  therefore,  be  a  pro- 
phylactic measure.  Removal  by  dental  instru- 
mentation need  not  be  described  here.  Oral 
hygiene — cleanliness — ^would  probably  tend  to  pre- 
vent their  formation. 

Some  Probable  Sources  of  Infection  That  May 
be  Avoided. — As  has  just  been  pointed  out,  there 
are  many  ways  in  which  lesions  favorable  for 
infection  with  endamebae  may  be  produced. 
Some  are  likely  to  be  produced  in  spite  of  care  to 
avoid  them.  It,  therefore,  becomes  important 
to  avoid  as  much  as  possible  introducing  end- 
amebae which  may  find  their  way  into  any  lesion 
present,  into  the  mouth.  There  is  no  evidence 
that  this  species  of  endamebae  live  and  reproduce 
anywhere  except  in  the  tissues  of  man,  so  far  as 
we  know,  nor  do  we  believe  it  at  all  probable 
that  such  is  the  case.  It,  therefore,  is  necessary 
that  infection  come  either  directly  or  indirectly 
from  another  infected  individual.  During  the 
many  years  required  for  the  sloughing  out  of  all 
the  teeth,  there  must  be  countless  millions  of 
endamebae  thrown  off  with  the  pus.  The  pus 
and  endamebae  are  mixed  with  the  saliva  in  the 
mouth.     This  infected  saliva  may  be  a  source  of 


PROPHYLAXIS  157 

infection  if  in  any  way  it  is  introduced  into  favor- 
able soil  for  the  endamebae.  So  far  as  we  are 
aware,  it  is  not  known  whether  EndamcEba  buccalis 
can  become  encysted  and  resist  drying  for  long 
periods  of  time,  but  it  is  known  that  certain  non- 
pathogenic species  of  amebae  retain  their  vitality 
in  a  dried  state  for  considerable  periods  of  time. 
The  amebae  cultivatable  from  hay  or  road  dust  are 
examples.  It  is  believed  that  cysts  of  the  end- 
amebae that  cause  amebic  dysentery  in  man  retain 
their  vitality  in  the  dried  state  for  considerable 
periods  of  time  also. 

Drinking  After  Others. — Whenever  a  person 
drinks  from  a  cup  or  other  container  he  touches 
the  sides  of  the  container  more  or  less  with  the 
lips.  Saliva  is  always  left  where  the  mouth 
touched.  It  is  quite  true  that  the  quantity  may 
be  very  small  in  many  instances,  but  it  may  con- 
tain many  microscopic  endamebae.  If  another 
person  drinks  and  places  his  lips  at  the  same  place, 
his  chances  of  getting  endamebae  on  his  lips  and 
in  his  mouth  are  good.  If  the  endamebae  retain 
their  vitality  under  such  conditions,  as  we  believe 
highly  probable,  one  might  be  infected  by  drinking 
from  a  cup  or  glass  that  had  been  infected  many 
hours  previously,  if  not  washed  between  times. 
Washing  removes  part  or  all  of  the  infection, 
depending  upon  its  thoroughness.     Washing  with 


158  ALVEOLODENTAL  PYORRHEA 

hot  water  kills  as  well  as  washes  away  the  infec- 
tion. The  public  drinking-cup  should,  of  course, 
be  avoided.  The  common  drinking-cup  or  glass 
in  the  home  is  also  dangerous.  Endamebae  ob- 
tained from  the  dearest  relative  can  produce  the 
disease  just  as  certainly  as  those  obtained  from  a 
stranger. 

Eating  After  Each  Other. — Eating  food  that 
has  been  bitten  by  others  or  using  knives,  forks, 
and  spoons  that  have  been  used  by  others  with- 
out proper  cleaning  may  likewise  be  a  source  of 
infection  and  therefore  should  be  avoided. 

Kissing. — Often,  in  kissing,  saliva  from  one  indi- 
vidual's lips  is  transferred  to  the  lips  of  another. 
This  saliva  is  quite  likely  to  contain  endamebae. 
Parents,  most  of  whom  have  the  infection,  could 
possibly  infect  their  children  in  this  way. 

Putting  Infected  Things  in  the  Mouth. — Putting 
in  the  mouth  articles  of  any  sort  that  have  been 
in  the  mouths  of  others  is  likely  to  transfer  end- 
amebae and  should  be  avoided.  Pencils,  money, 
papers,  etc.,  may  be  mentioned.  It  is  not  unusual 
to  see  a  parent,  nurse,  or  other  older  person  show 
a  child  how  to  blow  a  toy  or  other  instrument  and 
immediately  return  it,  infected,  to  the  child  to 
place  in  his  mouth.  Nearly  all  such  older  people 
have  pyorrhea  in  some  stage,  and  therefore  end- 
amebae in  their  saliva.     Such    things    should    be 


PROPHYLAXIS  159 

avoided,  and  children  should  be  taught  as  early 
as  possible  not  to  put  things  in  their  mouths  that 
had  been  in  the  mouths  of  others.  Nearest 
relatives  and  friends  are  not  to  be  excepted. 

A  possible  way  of  introducing  endamebae  into 
the  mouth  is  putting  things  that  have  been  con- 
taminated indirectly  into  the  mouth.  For  in- 
stance, some  person  having  a  bad  form  of  pyor- 
rhea may  in  some  way  contaminate  his  own  hands. 
With  them  he  may  handle  articles  of  various  sorts, 
which  in  turn  are  soon  handled  by  some  other 
individual.  The  latter  may  place  his  hands  on 
the  same  place  that  had  been  contaminated  and 
thus  contaminate  his  own  hands.  It  is  true  that 
the  amount  of  saliva  containing  endamebae  thus 
transferred  may  be  very  small,  but  during  the 
course  of  a  few  hours,  especially  in  public  places, 
a  person  would  stand  a  chance  to  touch  several 
contaminated  articles.  He  may  now  introduce 
the  contamination  into  his  mouth  in  a  number  of 
ways.  Many  people  put  their  hands  or  fingers 
to  their  lips  or  tongue  for  various  purposes,  or  often 
for  no  purpose,  many  times  during  each  day. 
Much  of  this  is  bad  habit  and  could  be  avoided. 

Eating  with  Unclean  Hands. — The  chances  of 
contaminating  the  hands  in  one  way  or  another 
are  so  great  that  they  may  be  presumed  to  be  con- 
taminated  at  most   any   time   unless   they  have 


i6o  ALVEOLODENTAL  PYORRHEA 

been  recently  well  washed.  It  is  not  uncommon  for 
people  to  go  to  the  table  and  eat  their  regular 
meals  without  washing  their  hands,  to  say  nothing 
of  handling  and  eating  various  things  between 
meals.     Such  habits  should  be  discontinued. 

Spitting. — Sputum  consists  of  saliva  and  secre- 
tion from  the  mouth  and  the  respiratory  tract. 
When  pyorrhea  exists,  there  are  more  or  less  end- 
amebae  contained  in  it.  In  some  cases  there  must 
be  very  large  numbers.  In  fact.  Smith,  Middle- 
ton,  and  Barrett  have  recently  found  Endamoeba 
buccalis  present  in  the  tonsils  in  a  considerable 
percentage  of  cases  of  chronic  tonsillitis.  The 
possibility  of  such  material  becoming  dried,  made 
into  dust,  and  this  transferred  through  various 
agencies  to  the  mouth  of  others,  thus  being  a 
source  of  infection,  is  probably  not  great,  but  may 
be  thought  of. 

Local  Use  of  Emetin  as  a  Prophylactic. — In  our 
early  experimental  work  on  pyorrhea  we  recog- 
nized the  necessity  of  preventing  reinfection  in 
cases  whose  endamebae  had  been  destroyed  by  the 
specific  treatment.  Otherwise,  reinfection  would 
surely  occur  long  before  the  lesions  in  most  cases 
could  heal.  We  naturally  selected  emetin  as  the 
drug  to  be  applied  locally  for  this  purpose.  On 
account  of  the  cost  of  the  alkaloid  at  that  time, 
we  thought  it  would  be  more  economic  and  prac- 


PROPHYLAXIS       .  i6i 

tical  to  employ  the  fluidextract  of  ipecac  contain- 
ing the  emetin  instead  of  the  pure  emetin.  The 
method  of  applying  it  was  to  have  the  patient 
apply  one  drop  of  the  fluidextract  of  ipecac  to  the 
wet  tooth-brush  and  brush  the  teeth  with  it  after 
first  having  brushed  them  to  clean  them.  The 
patient  was  instructed  to  force  the  solution  of 
ipecac  formed  in  the  mouth  between  the  teeth, 
and  to  spit  out  the  excess,  but  not  to  rinse  it  out. 
Our  idea  was  that  the  ipecac  probably  would  kill 
endamebae  that  may  have  been  introduced  through 
the  day,  but  that  were  located  only  superficially 
in  the  diseased  tissue.  To  determine  the  efficiency 
of  this  to  destroy  superficially  located  endamebae 
we  tried  it  on  a  number  of  patients  who  had  shallow 
lesions  with  endamebae.  In  a  number  of  them,  to 
our  great  satisfaction,  the  endamebae  disappeared 
from  shallow  lesions  in  a  few  days  and  the  lesions 
rapidly  healed.  This  was  without  any  other 
treatment.  If  the  local  use  of  ipecac  in  this  way 
destroys  endamebae  in  superficial  lesions  of  pyor- 
rhea, it  would  more  certainly  destroy  those  re- 
cently introduced  but  not  established. 

Fluidextract  of  ipecac  in  sufficient  concentra- 
tion causes  some  irritation  and  soreness  of  the 
mucous  membrane.  Many  patients,  when  in- 
structed to  use  one  drop,  think  that  if  that  small 
amount  will  do  good  more  will  do  more  good,  and 


i62  ALVEOLODENTAL  PYORRHEA 

therefore  use  enough  to  make  their  mouth  sore. 
A  more  practical  method  of  appHcation  that  we 
have  recently  employed  is  to  instruct  the  patient 
to  rinse  the  mouth  with  water  to  half  a  glassful  of 
which  one  or  two  drops  of  fluidextract  of  ipecac 
has  been  added.  The  amount  of  ipecac  present 
is  even  much  more  than  necessary  to  kill  all  end- 
amebae  with  which  it  comes  in  contact. 

More  recently  we  have  employed  a  solution  of 
emetin  hydrochlorid  in  water  instead  of  the  ipecac. 
The  prescription  usullay  given  the  patient  is: 

I^.  Emetin  hydrochlorid 5  grains 

Distilled  water i  ounce 

Mix.     Dispense  in  sprinkler-top  bottle. 

Label. — Put  one  or  two  drops  in  one-fourth  glass  water.    Use  as  a 
mouth-wash. 

The  five  grains  of  emetin  used  in  this  prescrip- 
tion cost  the  druggist  at  present  prices  about  50 
cents,  and  the  quantity  should  last  for  at  least  one 
year,  if  used  daily.  The  best  way  to  use  it  is  to 
take  some  of  the  dilute  solution  in  the  mouth  and 
force  it  back  and  forth  between  the  teeth.  Spit  it 
out  and  repeat.  The  object  is  to  wash  out  any- 
thing that  may  be  lodged  between  the  teeth  and 
to  leave  a  trace  of  the  solution  of  emetin  where  it 
is  likely  to  reach  any  endamebae  that  may  have 
recently  been  introduced. 

The  question  may  be  asked,  why  prescribe  the 
drug  in  concentrated  form  and  not  much  more 


PROPHYLAXIS  163 

diluted  ?  The  reply  is  that  there  is  no  necessity 
for  the  patient  to  buy  the  diluent  when  he  can  use 
water,  which  is  probably  the  best  and  costs  nothing. 
It  has  also  been  suggested  to  combine  the  emetin 
or  ipecac  with  other  more  pleasant  dentifrices, 
pastes,  powders,  etc.  It  is  our  opinion  that  they 
are  valueless,  and  often  harmful,  and  that  the 
after-effect  of  the  emetin  is  fully  as  pleasant  as 
any  of  them.  The  taste  is  bitter  at  first,  but  it  is 
not  an  unpleasant  bitter,  and  soon  passes  away. 
We  have  had  several  persons  to  tell  us  that  it 
produces  the  most  pleasant  effect  of  any  prepara- 
tion they  ever  used,  and  that  they  never  had  such 
a  pleasant,  clean  taste  in  the  mouth  as  is  produced 
by  the  use  of  emetin  or  ipecac.  In  the  light  of  our 
present  information,  ipecac  or,  preferably,  emetin, 
should  be  used  as  a  mouth-wash  once  every  day  or 
two  for  prophylaxis.  It  may  be  that  future  work 
may  show  that  some  other  method  of  using  it  is 
better  than  that  here  suggested,  but  this  is  prac- 
tical and  efficient. 

SUMMARY 

Endamoebae  buccalis  cannot  attack  normal 
tissue.  It  must  be  damaged.  Damaged  tissue, 
constituting  favorable  soil  for  endamebae,  may  be 
produced  by  hard  particles  of  food  forced  against 
the  gum,   picking  the   teeth,  vigorous  brushing, 


i64  ALVEOLODENTAL  PYORRHEA 

pressure  of  ill-fitting  crowns,  and  collections  of 
tartar  and  bacteria,  etc.     These  should  be  avoided. 

The  source  of  infection  is  pus  and  saliva  from 
the  mouth  of  some  other  person,  most  all  of  whom 
are  infected.  Drinking  and  eating  after  others 
should  be  avoided;  also  putting  anything  not 
known  to  be  free  from  contamination  into  the 
mouth. 

Rinse  the  mouth  once  a  day  (at  night)  with  a 
solution  of  fluidextract  of  ipecac  or  of  emetin  by 
forcing  the  solution  back  and  forth  between  the 
teeth.  The  solution  should  be  made  up  just  before 
use  by  adding  one  or  two  drops  of  fluidextract 
of  ipecac  or  one  or  two  drops  of  a  solution  of  5 
grains  of  emetin  in  one  ounce  of  water,  to  half  a 
glass  of  water. 

If  ipecac  or  emetin  was  used  in  this  manner 
from  childhood  through  life,  it  is  doubtful  whether 
the  individual  would  ever  get  the  disease. 


INDEX 


Alcresta  emetin,  135 

ipecac,  133 
Alveolar  bone,  anatomy,  2,  39 
process,  destruction  of,  63 
loss  of,  73 
Alveoli,  description  of,  39 
Alveolodental  pyorrhea,  contagious- 
ness of,  78 
course  of  disease,  54 
definition  of,  18 
diagnosis  of,  99 
etiology  of,  26 
historic  chapter,  19 
pathology  of,  38 
prophylaxis  of,  144 
symptomatology  of,  82 
treatment  of,  120 
Amebic  dysentery,   resemblance  of 
lesion  to  that  of  pyorrhea,  32 
ulcer,  similarity  to  pyorrhea,  32 
Amoeba  buccalis,  20 
gingivalis,  20 


Bacteria  transported  by  endame- 

ba,  50 
Bacterial   flora   contributing   factor 

in  pyorrhea,  36 
Bad  taste  in  mouth,  85 
Barrett  method  of  injecting  emetin 

into  pyorrhea  pockets,  132 
Bass  and  Johns  on  endameba,  22 
Bleeding  from  gums  as  a  symptom, 

83 
Blood,  loss  of,  in  pyorrhea,  67 
Breath,  foul,  85 


Brushing  the  teeth,  erosion  from,  153 
influence    in    etiology    of    py- 
orrhea, 35 
proper  method,  147,  150 


Calculus,  sahvary,  69 
treatment  of,  155 

serumal,  71 
Care  of  teeth,  144 
Cause  of  alveolodental  pyorrhea,  26 
Chiavaro,  27 

on  Endamceba,  21 
Contagiousness,  78 
Craig  on  ameba,«2i,  23 
Crowns,    artificial,    in    etiology    of 

pyorrhea,  36 


Definition,  17 

Dental  floss  a  contributing  factor  in 
pyorrhea,  34 
dangers  of,  146 

scaler,  100 

work,  ill-fitting,  154 
Dentin,  anatomy  of,  39 
Diagnosis,  99 

Differentiation  of  endamebae,  116 
Doflein  on  ameba,  20 
Drinking  after  others,  157 

cups,  79 


Eating  after  others,  158 

with  unclean  hands,  159 
Edema  of  gums,  93 


i6s 


i66 


INDEX 


Emetin,  action  on  endameba,  123 

Alcresta,  135 

description  of,  122 

dosage  of,  124 

injection  into  pyorrhea  pockets, 
129 

length  of  time  for  effect  of,  128 

local  effect  of,  126 

prophylactic  use  of,  160 

technic  of,  hypodermically,  126 

urticaria  from  use  of,  127 
Endamoeba,  appearance  of,  106 

buccalis,  description  of,  23 
historic,  19 

the   specific   cause  of  alveolo- 
dental  pyorrhea,  26 

constant  presence  of,  27 

differentiation  of,  116 

favorable  soil  for,  46 

food  of,  50 

living,  appearance  of,  1 12 

microscopic  examination,  loi 

reappearance  after  treatment,  143 

staining  of,  103 

the  cause  of  pyorrhea,  45 
Endocarditis  from  pyorrhea,  73 
Entamoeba,  20 

kartulisi,  21 
Erosion  of  teeth  from  brushing,  153 
Etiology,  26 

Examination,  microscopic,  for  end- 
ameba, lOI 

of  teeth, 100 


Food  a  factor  in  etiology,  47 
particles  in  etiology  of  pyorrhea, 

34 
Foul  breath,  85 
in  pyorrhea,  61 


Grassi  on  Amoeba  dentalis,  20 
Gros  on  ameba,  19 
Gum-boils,  95 


Gums,  bleeding  from,  83 
changes  in,  93 
retraction  of,  87 
soreness  of,  84 

Hands,  unclean,  eating  with,  159 

Historic,  19 

Hypodermic  use  of  emetin,  126 


Infection,  avoidance  of,  156 
modes  of,  78 

Instruments  for  examination,  100 

Ipecac,  Alcresta,  133 
description  of,  121 
prophylactic  use  of,  161 

Kartulis  on  ameba,  20 
Kissing,  i£8 
as  a  means  of  infection,  79 


Loose  teeth,  supporting  of,  142 
Looseness  of  teeth,  63,  88 


Malocclusion,  71,  89 
Microscope,  117 
Microscopic  examination,  loi 

apparatus  for,  116 
Middleton  and  Barrett  on  endameba, 

22 
Morbid  process  in  pyorrhea,  38 
Mouth,  bad  taste  in,  85 

putting  infected  articles  into,  158 

Odor  in  pyorrhea,  61 

Pastes,  tooth,  151 
Pathology,  38 

Peridental    membrane,    description 
of,  41 
infection  of,  46 


INDEX 


167 


Pockets,  pyorrhea,  formation  of,  54 

injection  of  emetin  into,  129 
Powders,  tooth,  151 
Prophylactic  use  of  emetin,  160 
Prophylaxis,  144 
Prowazek  on  ameba,  20 
Pus,  amount  lost  during  pyorrhea,  67 

discharge  of,  as  symptom,  86 
Pyorrhea.     For  subheads  see  Alveo. 
lodental  pyorrhea 

a  source  of  systemic  diseases,  73 

as  a  symptom,  86 

definition,  17 

lesion,  54 

pocket,  formation  of,  54 

injection  of  emetin  into,  129 


Reappearance  of  endameba,  143 
Redundant  tissue,  removal  of,  141 
Reinfection,  136 
Relapse,  136 

Retraction  of  gums,  58,  87 
Rheumatism  from  pyorrhea,  73 
Riggs'  disease,  definition,  17 
Rogers  on  emetin,  123 


Salivary  calculus,  69 
treatment  of,  155 

Scaling  of  roots  of  teeth,  140 

Septicemia  from  pyorrhea,  73 

Serumal  calculus,  71 

Smith,    A.    J.,    on    cultivation    of 
Endamoeba  buccalis,  24 

Smith  and  Barrett,  27 

on  Endamoeba  buccalis,  21,  24 

Soreness  of  gums,  84 

Specific  cause  of  alveolodental  py- 
orrhea, 26 

Spirochetes  in  mouth,  52 


Spitting,  160 

Staining  endamoeba,  103 

Sternberg  on  ameba,  20 

Symptomatology,  82 

Syringe    for   administering   emetin, 

126 
Syringes   for   injecting   emetin   into 

pyorrhea  pockets,  132 

Tartar  and  pyorrhea,  35 

removal  of,  149 
Taste,  bad,  in  mouth,  85 
Teeth,  care  of,  144 

change  of  position  of,  from  pyor- 
rhea, 71 

description  of,  39 

erosion  of,  from  brushing,  153 

examination  of,  lOO 

loose,  supporting  of,  142 

looseness  of,  63,  82,  88 

loss  of,  73 

soreness  of,  84 
Tooth,  description  of,  39 

pastes,  151 

powders,  151 

roots,  scaling  of,  140 

sensitiveness  of  neck  of,  87 
Tooth-brush,  dangers  of,  147,  150 
Toothpick,  47 

influence  in  etiology  of  pyorrhea, 

34 

use  of,  145 
Trauma,  influence  of,  in  etiology  of 

pyorrhea,  35 
Treatment,  120 

Urticaria  produced  by  emetin,  127 


Younger  dental  scaler,  100 


C^A^^ 


UNIVERSITY  OF  CALIFORNIA  LIBRARY 

Los  Angeles 
This  book  is  DUE  on  the  last  date  stamped  below. 


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